Murray Wiki - User contributions [en]

Sara Molinari, 29 Jan 2019

2019-01-27T21:56:01Z

Ahallera: /* Schedule */

Sara Molinari will visit Caltech on 29-30 Jan 2019.

=== Schedule ===

{| width=100% border=1
|- valign=top
| width=50% |
29 Jan (Tue):
* 8:30 am: Richard, 109 Steele Lab
* 9:00 am: seminar
* 10:00 am: Andrey (meet after seminar)
* 10:45 am: open
* 11:30 am: open
* 12:00 pm: Lunch with postdocs John McManus, Leo Green
* 1:00 pm: ELM discussion (Richard, James, Rory, ERDC?)
* 2:00 pm: Andy (meet at Richard's office)
* 2:45 pm: open
* 3:30 pm: open
* 4:15 pm: open
* 5:00 pm: done for the day
* 6:00 pm (or other): dinner with grad students (John Marken, Andy) (TBD)

| width=50% |
30 Jan (Wed):
* 9:00 am: Biocircuits group meeting
* 11:00 am: Hold: Niles?
* 11:45 am: open
* 12:30 pm: working lunch with James and Rory
* 1:45 pm: John Marken (103 Steele)
* 2:30 pm: Richard, 109 Steele Lab
* 3:00 pm: depart campus
|}

=== Talk ===

'''Engineering asymmetrical cell division into Escherichia coli'''

Sara Molinari, Rice University 
29 Jan (Tue) @ 9 am, 111 Keck

Multicellularity, in eukaryotic organisms, is ultimately responsible for most of the tissues features, such as controlling its shape and size, distributing biochemical, structural and reproductive tasks. Multicellularity is reached through asymmetrical cell division in which progenitor cells create a differentiated daughter cell while retaining their original phenotype. Here, we describe a synthetic genetic circuit for controlling asymmetrical cell division in Escherichia coli. Specifically, we engineered an inducible system that can bind and segregate plasmid DNA to a single position in the cell. Upon division, the co-localized plasmids are kept by one and only one of the daughter cells. The other daughter cell receives no plasmid DNA and is hence irreversibly differentiated from its sibling. In this way, we achieved asymmetric cell division though asymmetric plasmid partitioning. We used this system to achieve physical separation of genetically different cells. We also characterized an orthogonal inducible circuit that enables the simultaneous asymmetric partitioning of two plasmid species – resulting in pluripotent cells that have four distinct differentiated states. These results point the way towards engineering multicellular systems from prokaryotic hosts.

Sara Molinari, 29 Jan 2019

2019-01-26T20:47:44Z

Ahallera: /* Schedule */

SURF discussions, Jan 2019

2019-01-25T19:30:51Z

Ahallera: /* 28 Jan (Mon) */

Slots for talking with applicants and co-mentors about SURF projects. Please sign up for one of the slots below. All times are PST. __NOTOC__

In preparation for our conversation, please do the following:
* SURF students should work with their co-mentors to find a time the meeting/Skype call. (For Skype calls, co-mentors should initiate.)
* Please make sure you have read the material in the description of your project, so that you are prepared to talk about what the project is about and we can narrow in on the key ideas that will be the basis of your proposal
* Please take a look at the [[SURF GOTChA chart]] page, which is the format that we will use for the first iteration of your project proposal.

{| border=1 width=100%
|- valign=top
| width=25% |
==== 28 Jan (Mon) ====
* 5:00 pm PST: Victoria / Andy
* 5:30 pm PST: open
| width=25% |

==== 29 Jan (Tue) ====
* 12:00 pm PST: open
| width=25% |

==== 31 Jan (Thu) ====
* 12:00 pm PST: open
| width=25% |
==== 1 Feb (Fri) ====
* 11:00 am PST: Ludvig
<hr>
* 3:30 pm PST: open
* 4:00 pm PST: open
|}

The agenda for the phone call is (roughly):

# Description of the basic idea behind the project (based on applicant's understanding)
# Discussion about approaches, things to read, variations to consider, etc
# Discussion of the format of the proposal
# Questions and discussion about the process

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:18:51Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1).

[[File:ADH_evo_stability.png|600px|Image: 600 pixel]]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology. The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media. What's causing this physiological change, and can we characterize how burden forces this response?

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:17:57Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1).

[[File:ADH_evo_stability.png|600px|Image: 600 pixel]]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology. The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:05:50Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.png|600px|Image: 600 pixel]]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:05:33Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.png|100px|Image: 600 pixel]]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:05:24Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.png|100px|Image: 100 pixel]]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:05:15Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.png|100px|Image: 100 pixel]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time. ]]

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:03:29Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.png|Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time. ]]

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:02:59Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.png|thumb|Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time. ]]

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

File:ADH evo stability.png

2018-12-12T03:02:29Z

Ahallera:

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:00:21Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.jpg|thumb|Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time. ]]

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T03:00:09Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ASS_evo_stability.jpg|thumb|Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time. ]]

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T02:59:55Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ASS_DNAPEN.jpg|thumb|Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time. ]]

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T02:58:59Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:ADH_evo_stability.jpg]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-12T02:58:47Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[ADH_evo_stability.jpg]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:53:12Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[https://imgur.com/e9Awpw6]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:52:19Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''

Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:51:54Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:51:29Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

# '''1) Genetic circuit architecture and evolutionary'''

* Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

# '''2) Cellular response to synthetic burden'''

* We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

# '''3) Link expression of burdensome genes to ribosomal protein level'''

* Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:50:58Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
# https://pubs.acs.org/doi/10.1021/sb400055h
# http://www.nature.com/doifinder/10.1038/nmeth.4635
# http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:48:40Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
* https://pubs.acs.org/doi/10.1021/sb400055h
* http://www.nature.com/doifinder/10.1038/nmeth.4635
* http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:48:22Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

'''References'''
https://pubs.acs.org/doi/10.1021/sb400055h
http://www.nature.com/doifinder/10.1038/nmeth.4635
http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:47:45Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:47:13Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:47:01Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:45:15Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) Genetic circuit architecture and evolutionary'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.

* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:43:51Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.

'''1) How does the architecture of genetic circuit alter evolutionary stability?'''

Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)

'''2) Cellular response to synthetic burden'''

We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.

'''3) Link expression of burdensome genes to ribosomal protein level'''

Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.

* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:42:59Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.
[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.
1) How does the architecture of genetic circuit alter evolutionary stability?
Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)
2) Cellular response to synthetic burden
We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.
3) Link expression of burdensome genes to ribosomal protein level
Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''

There are no requirements for previous experience. The following could be useful depending on the project.

* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:42:26Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.
[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.
1) How does the architecture of genetic circuit alter evolutionary stability?
Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)
2) Cellular response to synthetic burden
We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.
3) Link expression of burdensome genes to ribosomal protein level
Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''
There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:42:10Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.
[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.
1) How does the architecture of genetic circuit alter evolutionary stability?
Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)
2) Cellular response to synthetic burden
We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.
3) Link expression of burdensome genes to ribosomal protein level
Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''
There are no requirements for previous experience. The following could be useful depending on the project.
* molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* time-lapse microscopy
* image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:41:40Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.
[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.
1) How does the architecture of genetic circuit alter evolutionary stability?
Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)
2) Cellular response to synthetic burden
We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.
3) Link expression of burdensome genes to ribosomal protein level
Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''
There are no requirements for previous experience. The following could be useful depending on the project.
* Molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* Time-lapse microscopy
* Image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:41:10Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.
[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.
1) How does the architecture of genetic circuit alter evolutionary stability?
Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)
2) Cellular response to synthetic burden
We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.
3) Link expression of burdensome genes to ribosomal protein level
Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience'''
There are no requirements for previous experience. The following could be useful depending on the project:
* Molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* Time-lapse microscopy
* Image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:40:32Z

Ahallera:

'''[[SURF 2019|2019 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception promised revolutions in practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program (Figure 1). This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.
[[File:/Users/andrewhalleran/Desktop/Screen Shot 2018-12-10 at 8.19.53 PM.png]

Figure 1: Cells containing an inducible activation circuit where addition of the small molecule salicylate drives sfYFP expression decrease in fluorescence over time.

The goal of this SURF project is to improve our understanding of the evolutionary stability of genetic circuits. This is a general aim and there are many potential projects that range from more biology focused (i.e. understanding the biology underpinning the stability of synthetic circuits) to more engineering focused (i.e. building circuits to improve lifetime). A few example projects are given below.
1) How does the architecture of genetic circuit alter evolutionary stability?
Compare different molecular implementations for the same desired behavior and see if there are differences in stability (e.g. repressor vs. activator for inducible transcription)
2) Cellular response to synthetic burden
We have preliminary data that shows once burdened cells go into stationary phase they have difficulty resuming exponential growth when they are transferred to fresh media.
3) Link expression of burdensome genes to ribosomal protein level
Previous work by Alon and Dekel (Shachrai et al., 2010, Mol Cell) demonstrated that synthetic protein expression is more costly when the cell has fewer ribosomes. This project would aim to link expression of synthetic circuit to the level of ribosomal proteins in the cell to minimize cellular burden.

'''Useful previous experience:'''
There are no requirements for previous experience. The following could be useful depending on the project:
* Molecular biology / cloning (PCR, bacterial transformation, culturing + miniprep, etc.)
* Time-lapse microscopy
* Image analysis
* statistics
* coding (python / matlab)
* mathematical modeling (ODEs, deterministic / stochastic simulations)

SURF 2019: Evolutionary Stability of Genetic Circuits

2018-12-11T04:38:59Z

Ahallera: Created page with "'''2019 SURF project description''' * Mentor: Richard Murray * Co-mentor: Andy Halleran ''' Evolutionary Stability of Genetic Circuits''' Synthetic biology’s..."

Chelsea Hu, Apr 2018

2018-04-05T19:12:29Z

Ahallera: /* Monday */

Chelsea Hu, a PhD student working with Julius Lucks at Northwestern, is going to be visiting on 9-10 Apr. Sign up below for a time to meet with her.

=== Monday ===
* ~9:15 am: Richard, 107 Steele
* 10 am: Biocircuits group meeting
* 12 pm: Lunch with current postdocs
* 1:30 pm: Andy
* 2:15 pm: Open
* 3:00 pm: Sam
* 4:30 pm: Open

=== Tuesday ===
* 9:30 am: Pradeep Ramesh <pramesh@caltech.edu>
* 10:15 am: Open
* 11:00 am: Open
* 12:00 pm: IST lunch bunch or lunch on your own
* Leave afternoon open for now
* 4:00 pm: Hold for BBE seminar
* 5:00 pm: Niles Pierce, 165 Broad
* 5:30 pm: Richard, 107 Steele

SURF discussions, Jan 2018

2018-01-22T20:08:35Z

Ahallera: /* 23 Jan (Tue) */

Slots for talking with applicants and co-mentors about SURF projects. Please sign up for one of the slots below. All times are PST. __NOTOC__

In preparation for our conversation, please do the following:
* SURF students should work with their co-mentors to find a time the meeting/Skype call. (For Skype calls, co-mentors should initiate.)
* Please make sure you have read the material in the description of your project, so that you are prepared to talk about what the project is about and we can narrow in on the key ideas that will be the basis of your proposal
* Please take a look at the [[SURF GOTChA chart]] page, which is the format that we will use for the first iteration of your project proposal.

{| border=1
|- valign=top
| width=30% |
==== 23 Jan (Tue) ====
* 1:00 pm PST: open
<hr>
* 4:00 pm PST: Andrey/ Sanjana
* 4:30 pm PST: open
<hr>
* 6:00 pm PST: Andy/Emanuel
* 6:30 pm PST: open
| width=30% |

==== 24 Jan (Wed) ====
* 7:30 am PST: open (hold for India/Europe)
* 8:00 am PST: Rory/Elin
<hr>
*12:15 pm PST: Filip / Jin
*12:45 pm PST: open (if needed)
<hr>
* 4:30 pm PST: Reed / Leah
* 5:00 pm PST: open
* 5:30 pm PST: open
|}

The agenda for the phone call is (roughly):

# Description of the basic idea behind the project (based on applicant's understanding)
# Discussion about approaches, things to read, variations to consider, etc
# Discussion of the format of the proposal
# Questions and discussion about the process

SURF 2018: Evolutionary Stability of Genetic Circuits

2017-12-15T21:54:58Z

Ahallera:

'''[[SURF 2018|2018 SURF]] project description'''
* Mentor: Richard Murray
* Co-mentor: Andy Halleran

''' Evolutionary Stability of Genetic Circuits'''
Synthetic biology’s heralded inception 15 years ago promised synthetic biology would revolutionize practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program. This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

The goal of this SURF project is to characterize the mutational stability of existing synthetic circuits, followed by design and implementation of biomolecular feedback systems to improve circuit lifetimes. SURF students would work on developing techniques for characterizing mutational stability (flow cytometry, high throughput sequencing, etc.), mathematical modeling of the escape phenomenon (time to mutation, effect of load and circuit copy number on time to escape), and gain experience in synthetic circuit design and implementation.

'''Useful previous experience:'''
Molecular biology (cloning, heterologous gene expression, etc.), coding in python / matlab / etc., math modeling, deterministic / stochastic simulations

'''Relevant background literature:'''
https://www.biorxiv.org/content/early/2017/08/20/177030

http://www.sciencedirect.com/science/article/pii/S1097276510003266

SURF 2018: Evolutionary Stability of Genetic Circuits

2017-12-15T21:51:36Z

Ahallera: Created page with "Synthetic biology’s heralded inception 15 years ago promised synthetic biology would revolutionize practically every field, from agriculture and manufacturing to medicine. H..."

Synthetic biology’s heralded inception 15 years ago promised synthetic biology would revolutionize practically every field, from agriculture and manufacturing to medicine. However, all synthetic biology faces an uphill battle: synthetic circuits require host resources, inevitably slowing host growth. Therefore, mutants that disable the synthetic circuit grow faster than cells faithfully carrying out the programmed function. This causes mutants to outcompete engineered cells, bringing an end to the synthetic program. This universal feature of synthetic biology imposes a limit on the lifetime of programmed cellular functions. Improving the lifetime of synthetic circuits is of fundamental importance to the field of synthetic biology.

The goal of this SURF project is to characterize the mutational stability of existing synthetic circuits, followed by design and implementation of biomolecular feedback systems to improve circuit lifetimes. SURF students would work on developing techniques for characterizing mutational stability (flow cytometry, high throughput sequencing, etc.), mathematical modeling of the escape phenomenon (time to mutation, effect of load and circuit copy number on time to escape), and gain experience in synthetic circuit design and implementation.

Useful previous experience:
Molecular biology (cloning, heterologous gene expression, etc.), coding in python / matlab / etc., math modeling, deterministic / stochastic simulations

Background literature:
https://www.biorxiv.org/content/early/2017/08/20/177030

http://www.sciencedirect.com/science/article/pii/S1097276510003266

Group Schedule, Fall 2017

2017-11-14T00:42:15Z

Ahallera: /* Week 10: 27 Nov - 1 Dec */

This page contains information about various upcoming events that are of interest to the group. __NOTOC__
{| width=60%
|- valign=top
| width=50% |
* [[Schedule|Richard's calendar (travel)]]
| width=50% |
* [[Group Schedule, Summer 2017]]
|}

The schedule for group and subgroup meetings is given below. Contact Richard if you need to change the schedule. Unless otherwise noted, here are the locations of the meetings:

:{| width=100%
|- valign=top
| width=30% |
* Biocircuits subgroup - 111 Keck
| width=30% |
* NCS subgroup - 110 Steele or 243 ANB
| width=30% |
* Group meetings - 213 ANB
|}

{| width=100% border=1
|- valign=top

| width=25% |
=== Week 1: 25 Sep.- 29 Sep ===
'''Biocircuits: Tue, 10a-12p'''
* Miroslav
* Wolfgang
'''NCS: Wed, 10:30a-12p'''
* Ioannis


| width=25% |
=== Week 2: 2 Oct - 6 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* Ania
* Leo
'''NCS: Wed, 10:30a-12p'''
* Karan Kalsi (PNNL)


| width=25% |
=== Week 3: 9 Oct - 13 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* James
* Vipul
'''NCS: Wed, 10:30a-12p'''
* Jin


| width=25% |
=== Week 4: 16 Oct - 20 Oct ===
'''Biocircuits: <s>Tue</s> Wed, 10a-12p'''
* Mark
* Anandh
'''NCS: Wed, <s>10:30a-12p</s> 3:45p-5p'''
* Jonathan
<hr>
* Tuesday: WASP student visit, 9a-12p
* Friday: Mary Dunlop visit

|- valign=top

| width=25% |
=== Week 5: 23 Oct - 27 Oct ===
'''Biocircuits: Mon, 10a-12p'''
* Andrey
* Cindy
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 6: 30 Oct - 3 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* Sam
* Reed
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sofie


| width=25% |

=== Week 7: 6 Nov - 10 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* William
* <s>Shan</s>
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sumanth


| width=25% |

=== Week 8: 13 Nov - 17 Nov ===
'''NCS: Mon, 10:30a-12p'''
* Richard C
'''Biocircuits: Tue, 10a-12p'''
* Michaelle
* Joe M
<hr>
* Richard out of town Wed-Fri

|- valign=top

| width=25% |

=== Week 9: 20 Nov - 24 Nov ===
'''Biocircuits: Tue, 10a-12p'''
* Shan
* Rory
'''NCS: Tue, 1:30p-3p'''
* Karena
* Note: this meeting may shift to Mon
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 10: 27 Nov - 1 Dec ===
'''Biocircuits: Mon, 10a-12p, 114 Steele'''
* Andy
* Gloria Ha
'''NCS: Wed, 10:30a-12p'''
* Tung Phan
* Note: this meeting may shift to Fri


| width=25% |

=== Week 11: 4 Dec - 8 Dec ===
'''Biocircuits: Mon, 11a-12p'''
* Lab cleanup
'''NCS: Mon, 1:30p-3p'''
* Hold: Petter Nilsson
'''Biocircuits: Tue, 10a-12p, 114 Steele'''
* Alex
* Zoila
* Junedh


| width=25% |

=== Week 12: 11 Dec - 15 Dec ===
* No meetings this week
* Richard out of town Mon-Fri


|}

Group Schedule, Fall 2017

2017-11-14T00:42:05Z

Ahallera: /* Week 9: 20 Nov - 24 Nov */

This page contains information about various upcoming events that are of interest to the group. __NOTOC__
{| width=60%
|- valign=top
| width=50% |
* [[Schedule|Richard's calendar (travel)]]
| width=50% |
* [[Group Schedule, Summer 2017]]
|}

The schedule for group and subgroup meetings is given below. Contact Richard if you need to change the schedule. Unless otherwise noted, here are the locations of the meetings:

:{| width=100%
|- valign=top
| width=30% |
* Biocircuits subgroup - 111 Keck
| width=30% |
* NCS subgroup - 110 Steele or 243 ANB
| width=30% |
* Group meetings - 213 ANB
|}

{| width=100% border=1
|- valign=top

| width=25% |
=== Week 1: 25 Sep.- 29 Sep ===
'''Biocircuits: Tue, 10a-12p'''
* Miroslav
* Wolfgang
'''NCS: Wed, 10:30a-12p'''
* Ioannis


| width=25% |
=== Week 2: 2 Oct - 6 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* Ania
* Leo
'''NCS: Wed, 10:30a-12p'''
* Karan Kalsi (PNNL)


| width=25% |
=== Week 3: 9 Oct - 13 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* James
* Vipul
'''NCS: Wed, 10:30a-12p'''
* Jin


| width=25% |
=== Week 4: 16 Oct - 20 Oct ===
'''Biocircuits: <s>Tue</s> Wed, 10a-12p'''
* Mark
* Anandh
'''NCS: Wed, <s>10:30a-12p</s> 3:45p-5p'''
* Jonathan
<hr>
* Tuesday: WASP student visit, 9a-12p
* Friday: Mary Dunlop visit

|- valign=top

| width=25% |
=== Week 5: 23 Oct - 27 Oct ===
'''Biocircuits: Mon, 10a-12p'''
* Andrey
* Cindy
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 6: 30 Oct - 3 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* Sam
* Reed
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sofie


| width=25% |

=== Week 7: 6 Nov - 10 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* William
* <s>Shan</s>
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sumanth


| width=25% |

=== Week 8: 13 Nov - 17 Nov ===
'''NCS: Mon, 10:30a-12p'''
* Richard C
'''Biocircuits: Tue, 10a-12p'''
* Michaelle
* Joe M
<hr>
* Richard out of town Wed-Fri

|- valign=top

| width=25% |

=== Week 9: 20 Nov - 24 Nov ===
'''Biocircuits: Tue, 10a-12p'''
* Shan
* Rory
'''NCS: Tue, 1:30p-3p'''
* Karena
* Note: this meeting may shift to Mon
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 10: 27 Nov - 1 Dec ===
'''Biocircuits: Mon, 10a-12p, 114 Steele'''
* Shan
* Gloria Ha
'''NCS: Wed, 10:30a-12p'''
* Tung Phan
* Note: this meeting may shift to Fri


| width=25% |

=== Week 11: 4 Dec - 8 Dec ===
'''Biocircuits: Mon, 11a-12p'''
* Lab cleanup
'''NCS: Mon, 1:30p-3p'''
* Hold: Petter Nilsson
'''Biocircuits: Tue, 10a-12p, 114 Steele'''
* Alex
* Zoila
* Junedh


| width=25% |

=== Week 12: 11 Dec - 15 Dec ===
* No meetings this week
* Richard out of town Mon-Fri


|}

Group Schedule, Fall 2017

2017-11-02T23:12:07Z

Ahallera: /* Week 8: 13 Nov - 17 Nov */

This page contains information about various upcoming events that are of interest to the group. __NOTOC__
{| width=60%
|- valign=top
| width=50% |
* [[Schedule|Richard's calendar (travel)]]
| width=50% |
* [[Group Schedule, Summer 2017]]
|}

The schedule for group and subgroup meetings is given below. Contact Richard if you need to change the schedule. Unless otherwise noted, here are the locations of the meetings:

:{| width=100%
|- valign=top
| width=30% |
* Biocircuits subgroup - 111 Keck
| width=30% |
* NCS subgroup - 110 Steele or 243 ANB
| width=30% |
* Group meetings - 213 ANB
|}

{| width=100% border=1
|- valign=top

| width=25% |
=== Week 1: 25 Sep.- 29 Sep ===
'''Biocircuits: Tue, 10a-12p'''
* Miroslav
* Wolfgang
'''NCS: Wed, 10:30a-12p'''
* Ioannis


| width=25% |
=== Week 2: 2 Oct - 6 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* Ania
* Leo
'''NCS: Wed, 10:30a-12p'''
* Karan Kalsi (PNNL)


| width=25% |
=== Week 3: 9 Oct - 13 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* James
* Vipul
'''NCS: Wed, 10:30a-12p'''
* Jin


| width=25% |
=== Week 4: 16 Oct - 20 Oct ===
'''Biocircuits: <s>Tue</s> Wed, 10a-12p'''
* Mark
* Anandh
'''NCS: Wed, <s>10:30a-12p</s> 3:45p-5p'''
* Jonathan
<hr>
* Tuesday: WASP student visit, 9a-12p
* Friday: Mary Dunlop visit

|- valign=top

| width=25% |
=== Week 5: 23 Oct - 27 Oct ===
'''Biocircuits: Mon, 10a-12p'''
* Andrey
* Cindy
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 6: 30 Oct - 3 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* Sam
* Reed
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sofie


| width=25% |

=== Week 7: 6 Nov - 10 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* William
* Shan
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sumanth


| width=25% |

=== Week 8: 13 Nov - 17 Nov ===
'''NCS: Mon, 10:30a-12p'''
* Richard C
'''Biocircuits: Tue, 10a-12p'''
* Michaelle
* Joe M
<hr>
* Richard out of town Wed-Fri

|- valign=top

| width=25% |

=== Week 9: 20 Nov - 24 Nov ===
'''Biocircuits: Tue, 10a-12p'''
* Andy
* Rory
'''NCS: Tue, 1:30p-3p'''
* Karena
* Note: this meeting may shift to Mon
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 10: 27 Nov - 1 Dec ===
'''Biocircuits: Mon, 10a-12p, 114 Steele'''
* Hold: rotation student
* Hold: undergrad
* Note: this meeting may shift to Mon
'''NCS: Wed, 10:30a-12p'''
* Tung Phan
* Note: this meeting may shift to Fri


| width=25% |

=== Week 11: 4 Dec - 8 Dec ===
'''Biocircuits: Mon, 11a-12p'''
* Lab cleanup
'''NCS: Mon, 1:30p-3p'''
* Hold: Petter Nilsson
'''Biocircuits: Tue, 10a-12p, 114 Steele'''
* Hold: rotation student
* Hold: undergraduate


| width=25% |
=== Week 12: 11 Dec - 15 Dec ===
* No meetings this week
* Richard out of town Mon-Fri


|}

Group Schedule, Fall 2017

2017-11-02T23:11:53Z

Ahallera: /* Week 9: 20 Nov - 24 Nov */

This page contains information about various upcoming events that are of interest to the group. __NOTOC__
{| width=60%
|- valign=top
| width=50% |
* [[Schedule|Richard's calendar (travel)]]
| width=50% |
* [[Group Schedule, Summer 2017]]
|}

The schedule for group and subgroup meetings is given below. Contact Richard if you need to change the schedule. Unless otherwise noted, here are the locations of the meetings:

:{| width=100%
|- valign=top
| width=30% |
* Biocircuits subgroup - 111 Keck
| width=30% |
* NCS subgroup - 110 Steele or 243 ANB
| width=30% |
* Group meetings - 213 ANB
|}

{| width=100% border=1
|- valign=top

| width=25% |
=== Week 1: 25 Sep.- 29 Sep ===
'''Biocircuits: Tue, 10a-12p'''
* Miroslav
* Wolfgang
'''NCS: Wed, 10:30a-12p'''
* Ioannis


| width=25% |
=== Week 2: 2 Oct - 6 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* Ania
* Leo
'''NCS: Wed, 10:30a-12p'''
* Karan Kalsi (PNNL)


| width=25% |
=== Week 3: 9 Oct - 13 Oct ===
'''Biocircuits: Tue, 10a-12p'''
* James
* Vipul
'''NCS: Wed, 10:30a-12p'''
* Jin


| width=25% |
=== Week 4: 16 Oct - 20 Oct ===
'''Biocircuits: <s>Tue</s> Wed, 10a-12p'''
* Mark
* Anandh
'''NCS: Wed, <s>10:30a-12p</s> 3:45p-5p'''
* Jonathan
<hr>
* Tuesday: WASP student visit, 9a-12p
* Friday: Mary Dunlop visit

|- valign=top

| width=25% |
=== Week 5: 23 Oct - 27 Oct ===
'''Biocircuits: Mon, 10a-12p'''
* Andrey
* Cindy
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 6: 30 Oct - 3 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* Sam
* Reed
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sofie


| width=25% |

=== Week 7: 6 Nov - 10 Nov ===
'''Biocircuits: Wed, 10a-12p'''
* William
* Shan
'''NCS: Wed, 3:45p-5p, 243 ANB'''
* Sumanth


| width=25% |

=== Week 8: 13 Nov - 17 Nov ===
'''NCS: Mon, 10:30a-12p'''
* Richard C
'''Biocircuits: Tue, 10a-12p'''
* Michaelle
* Andy
<hr>
* Richard out of town Wed-Fri

|- valign=top

| width=25% |
=== Week 9: 20 Nov - 24 Nov ===
'''Biocircuits: Tue, 10a-12p'''
* Andy
* Rory
'''NCS: Tue, 1:30p-3p'''
* Karena
* Note: this meeting may shift to Mon
<hr>
* Richard out of town Tue-Fri

| width=25% |

=== Week 10: 27 Nov - 1 Dec ===
'''Biocircuits: Mon, 10a-12p, 114 Steele'''
* Hold: rotation student
* Hold: undergrad
* Note: this meeting may shift to Mon
'''NCS: Wed, 10:30a-12p'''
* Tung Phan
* Note: this meeting may shift to Fri


| width=25% |

=== Week 11: 4 Dec - 8 Dec ===
'''Biocircuits: Mon, 11a-12p'''
* Lab cleanup
'''NCS: Mon, 1:30p-3p'''
* Hold: Petter Nilsson
'''Biocircuits: Tue, 10a-12p, 114 Steele'''
* Hold: rotation student
* Hold: undergraduate


| width=25% |
=== Week 12: 11 Dec - 15 Dec ===
* No meetings this week
* Richard out of town Mon-Fri


|}

Mary Dunlop, Oct 2017

2017-10-19T09:15:20Z

Ahallera: /* Topic #2: feedback control of biological systems */

Mary Dunlop will visit Caltech on 19-20 Oct 2017. __NOTOC__

== Topics ==

Richard will organize a set of discussions with Mary on different topics. If you are interested in joining in the discussions, sign up below. You should put your name and any constraints on your time.

{| border=1
|- valign=top
| width=33% |
==== Topic #1: mutational robustness ====
* Richard - available 1-5 pm
* Anandh - 24/7/365
* Rory - 1-5pm (skype)
* Reed - available 1-5pm
* Andy - available 2-5pm
| width=33% |

==== Topic #2: feedback control of biological systems ====
* Richard - available 1-5 pm
* Ania - 1pm - 4pm
* Vipul - available 1-5p
* Reed - available 1-5pm
* Andy - available 2-5pm
* Name - availability
| width=33% |

==== Topic #3: TX-TL (modeling and experiments) ====
* Richard - available 1-5 pm
* William - busy 1-4 pm
* Vipul - available 1-5p
* Name - availability
|}

==== Additional topics ====
* If you have an additional topic you would like to discuss, but it here.

== Schedule ==
To be filled out later.

==== Thursday ====
* 11:00 am: Seminar in Gates-Thomas

=== Friday ===
* 8:45 am: Open
* 9:30 am: Ania
* 10:15 am: Vipul/Anandh (system ID etc)
* 11 am - 2 pm: off campus
* 2-5 pm: group discussions (sign up above)
* 5:00 pm: Done for the day

Mary Dunlop, Oct 2017

2017-10-19T09:14:55Z

Ahallera: /* Topic #1: mutational robustness */

Mary Dunlop will visit Caltech on 19-20 Oct 2017. __NOTOC__

== Topics ==

Richard will organize a set of discussions with Mary on different topics. If you are interested in joining in the discussions, sign up below. You should put your name and any constraints on your time.

{| border=1
|- valign=top
| width=33% |
==== Topic #1: mutational robustness ====
* Richard - available 1-5 pm
* Anandh - 24/7/365
* Rory - 1-5pm (skype)
* Reed - available 1-5pm
* Andy - available 2-5pm
| width=33% |

==== Topic #2: feedback control of biological systems ====
* Richard - available 1-5 pm
* Ania - 1pm - 4pm
* Vipul - available 1-5p
* Reed - available 1-5pm
* Name - availability
| width=33% |

==== Topic #3: TX-TL (modeling and experiments) ====
* Richard - available 1-5 pm
* William - busy 1-4 pm
* Vipul - available 1-5p
* Name - availability
|}

==== Additional topics ====
* If you have an additional topic you would like to discuss, but it here.

== Schedule ==
To be filled out later.

==== Thursday ====
* 11:00 am: Seminar in Gates-Thomas

=== Friday ===
* 8:45 am: Open
* 9:30 am: Ania
* 10:15 am: Vipul/Anandh (system ID etc)
* 11 am - 2 pm: off campus
* 2-5 pm: group discussions (sign up above)
* 5:00 pm: Done for the day

May 2017 meeting schedule

2017-05-09T02:09:28Z

Ahallera: /* 28 May (Sun) */

Richard will be in town several different times in May. Please sign up for a time to meet below. Please note that these are likely the last "sabbatical" meetings until Richard returns to Pasadena in early July. __NOTOC__

{| border=1 width=100%
|- valign=top
| width=33% |
| width=33% |
==== 15 May (Mon) ====
* 9:30 am: Open
* 10:15 am: Open
* 11:00 am: Faculty meeting
* 11:30 am: Andy
* 12:15 pm: Lunch
* 1:30 pm: Sam
* 2:15 pm: Reed
* 3:00 pm: Open
* 3:45 pm: Break
* 4:00 pm: Namita
* 4:45 pm: Ania
* 5:30 pm: Anandh
* 6:15 pm: Done for the day

| width=33% |

==== 16 May (Tue)====
* 9:30 am: Yong
* 10:15 am: Tung
* 11:00 am: Faculty meeting
* 12:00 pm: Lunch
* 1:30 pm: Depart
* 12:00 pm: Lunch
* 1:30 pm: Depart

|- valign=top
| width=33% |

====21 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: Open
* 3:15 pm: Karena
* 4:00 pm: Break
* 4:15 pm: Open
* 5:00 pm: Open
* 5:45 pm: Open
* 6:30 pm: Done for the day

| width=33% |

==== 22 May (Mon) ====
* 10:15 am: Mark
* 11:00 am: Cindy
* 11:45 am: Lunch
* 12:00 pm: DARPA BioCon meeting
* 2:00 pm: Swati + Reed
* 2:45 pm: Off campus
* 4:15 pm: James
* 5:00 pm: Non-Caltech meetings
* 6:30 pm: Done for the day

| width=33% |

==== 23 May (Tue) ====
* 9:30 am: Faculty discussion
* 10:30 am: Hold (Susan)
* 11:30 am: Lunch
* 12:00 pm: Telecon
* 1:00 pm: Anu thesis defense
* 3:00 pm: Terri (?)
* 3:30 pm: Depart

|- valign=top
| width=33% |

====28 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: George
* 3:15 pm: Andy
* 4:00 pm: Done for the day
| width=33% |

====29 May (Mon) ====
* 1:45 pm: Open (if needed)
* 2:30 pm: Open (if needed)
* 3:15 pm: Sumanth
* 4:00 pm: Done for the day
| width=33% |

==== 30 May (Tue) ====
* 9:30 am: Shan
* 10:15 am: Shaobin
* 11:00 am: Stepan seminar
* 12:00 pm: Lunch
* 1:30 pm: Namita
* 2:15 pm: Andrey
* 3:00 pm: Depart
|}

May 2017 meeting schedule

2017-05-09T02:09:17Z

Ahallera: /* 21 May (Sun) */

Richard will be in town several different times in May. Please sign up for a time to meet below. Please note that these are likely the last "sabbatical" meetings until Richard returns to Pasadena in early July. __NOTOC__

{| border=1 width=100%
|- valign=top
| width=33% |
| width=33% |
==== 15 May (Mon) ====
* 9:30 am: Open
* 10:15 am: Open
* 11:00 am: Faculty meeting
* 11:30 am: Andy
* 12:15 pm: Lunch
* 1:30 pm: Sam
* 2:15 pm: Reed
* 3:00 pm: Open
* 3:45 pm: Break
* 4:00 pm: Namita
* 4:45 pm: Ania
* 5:30 pm: Anandh
* 6:15 pm: Done for the day

| width=33% |

==== 16 May (Tue)====
* 9:30 am: Yong
* 10:15 am: Tung
* 11:00 am: Faculty meeting
* 12:00 pm: Lunch
* 1:30 pm: Depart
* 12:00 pm: Lunch
* 1:30 pm: Depart

|- valign=top
| width=33% |

====21 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: Open
* 3:15 pm: Karena
* 4:00 pm: Break
* 4:15 pm: Open
* 5:00 pm: Open
* 5:45 pm: Open
* 6:30 pm: Done for the day

| width=33% |

==== 22 May (Mon) ====
* 10:15 am: Mark
* 11:00 am: Cindy
* 11:45 am: Lunch
* 12:00 pm: DARPA BioCon meeting
* 2:00 pm: Swati + Reed
* 2:45 pm: Off campus
* 4:15 pm: James
* 5:00 pm: Non-Caltech meetings
* 6:30 pm: Done for the day

| width=33% |

==== 23 May (Tue) ====
* 9:30 am: Faculty discussion
* 10:30 am: Hold (Susan)
* 11:30 am: Lunch
* 12:00 pm: Telecon
* 1:00 pm: Anu thesis defense
* 3:00 pm: Terri (?)
* 3:30 pm: Depart

|- valign=top
| width=33% |

====28 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: George
* 3:15 pm: Open
* 4:00 pm: Done for the day
| width=33% |

====29 May (Mon) ====
* 1:45 pm: Open (if needed)
* 2:30 pm: Open (if needed)
* 3:15 pm: Sumanth
* 4:00 pm: Done for the day
| width=33% |

==== 30 May (Tue) ====
* 9:30 am: Shan
* 10:15 am: Shaobin
* 11:00 am: Stepan seminar
* 12:00 pm: Lunch
* 1:30 pm: Namita
* 2:15 pm: Andrey
* 3:00 pm: Depart
|}

May 2017 meeting schedule

2017-05-09T02:09:10Z

Ahallera: /* 15 May (Mon) */

Richard will be in town several different times in May. Please sign up for a time to meet below. Please note that these are likely the last "sabbatical" meetings until Richard returns to Pasadena in early July. __NOTOC__

{| border=1 width=100%
|- valign=top
| width=33% |
| width=33% |
==== 15 May (Mon) ====
* 9:30 am: Open
* 10:15 am: Open
* 11:00 am: Faculty meeting
* 11:30 am: Andy
* 12:15 pm: Lunch
* 1:30 pm: Sam
* 2:15 pm: Reed
* 3:00 pm: Open
* 3:45 pm: Break
* 4:00 pm: Namita
* 4:45 pm: Ania
* 5:30 pm: Anandh
* 6:15 pm: Done for the day

| width=33% |

==== 16 May (Tue)====
* 9:30 am: Yong
* 10:15 am: Tung
* 11:00 am: Faculty meeting
* 12:00 pm: Lunch
* 1:30 pm: Depart
* 12:00 pm: Lunch
* 1:30 pm: Depart

|- valign=top
| width=33% |

====21 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: Andy
* 3:15 pm: Karena
* 4:00 pm: Break
* 4:15 pm: Open
* 5:00 pm: Open
* 5:45 pm: Open
* 6:30 pm: Done for the day

| width=33% |

==== 22 May (Mon) ====
* 10:15 am: Mark
* 11:00 am: Cindy
* 11:45 am: Lunch
* 12:00 pm: DARPA BioCon meeting
* 2:00 pm: Swati + Reed
* 2:45 pm: Off campus
* 4:15 pm: James
* 5:00 pm: Non-Caltech meetings
* 6:30 pm: Done for the day

| width=33% |

==== 23 May (Tue) ====
* 9:30 am: Faculty discussion
* 10:30 am: Hold (Susan)
* 11:30 am: Lunch
* 12:00 pm: Telecon
* 1:00 pm: Anu thesis defense
* 3:00 pm: Terri (?)
* 3:30 pm: Depart

|- valign=top
| width=33% |

====28 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: George
* 3:15 pm: Open
* 4:00 pm: Done for the day
| width=33% |

====29 May (Mon) ====
* 1:45 pm: Open (if needed)
* 2:30 pm: Open (if needed)
* 3:15 pm: Sumanth
* 4:00 pm: Done for the day
| width=33% |

==== 30 May (Tue) ====
* 9:30 am: Shan
* 10:15 am: Shaobin
* 11:00 am: Stepan seminar
* 12:00 pm: Lunch
* 1:30 pm: Namita
* 2:15 pm: Andrey
* 3:00 pm: Depart
|}

May 2017 meeting schedule

2017-05-08T18:12:37Z

Ahallera: /* 21 May (Sun) */

Richard will be in town several different times in May. Please sign up for a time to meet below. Please note that these are likely the last "sabbatical" meetings until Richard returns to Pasadena in early July. __NOTOC__

{| border=1 width=100%
|- valign=top
| width=33% |
| width=33% |
==== 15 May (Mon) ====
* 9:30 am: Open
* 10:15 am: Open
* 11:00 am: Faculty meeting
* 11:30 am: Open
* 12:15 pm: Lunch
* 1:30 pm: Open
* 2:15 pm: Reed
* 3:00 pm: Open
* 3:45 pm: Break
* 4:00 pm: Namita
* 4:45 pm: Ania
* 5:30 pm: Anandh
* 6:15 pm: Done for the day

| width=33% |

==== 16 May (Tue)====
* 9:30 am: Yong
* 10:15 am: Tung
* 11:00 am: Faculty meeting
* 12:00 pm: Lunch
* 1:30 pm: Depart
* 12:00 pm: Lunch
* 1:30 pm: Depart

|- valign=top
| width=33% |

====21 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: Andy
* 3:15 pm: Open
* 4:00 pm: Break
* 4:15 pm: Open
* 5:00 pm: Open
* 5:45 pm: Open
* 6:30 pm: Done for the day

| width=33% |

==== 22 May (Mon) ====
* 10:15 am: Mark
* 11:00 am: Cindy
* 11:45 am: Lunch
* 12:00 pm: DARPA BioCon meeting
* 2:00 pm: Swati + Reed
* 2:45 pm: Off campus
* 4:15 pm: James
* 5:00 pm: Non-Caltech meetings
* 6:30 pm: Done for the day

| width=33% |

==== 23 May (Tue) ====
* 9:30 am: Faculty discussion
* 10:30 am: Hold (Susan)
* 11:30 am: Lunch
* 12:00 pm: Telecon
* 1:00 pm: Anu thesis defense
* 3:00 pm: Terri (?)
* 3:30 pm: Depart

|- valign=top
| width=33% |

====28 May (Sun) ====
* 1:45 pm: Open
* 2:30 pm: George
* 3:15 pm: Open
* 4:00 pm: Done for the day
| width=33% |

====29 May (Mon) ====
* 1:45 pm: Open (if needed)
* 2:30 pm: Open (if needed)
* 3:15 pm: Open (if needed)
* 4:00 pm: Done for the day
| width=33% |

==== 30 May (Tue) ====
* 9:30 am: Shan
* 10:15 am: Shaobin
* 11:00 am: Stepan seminar
* 12:00 pm: Lunch
* 1:30 pm: Namita
* 2:15 pm: Andrey
* 3:00 pm: Depart
|}