In this section

Research

Biological systems - including the simplest cells - exhibit a broad range of functions to thrive in their environment. Research in the Imperial College Centre for Synthetic Biology is focused on the possibility of engineering the underlying biochemical processes to solve many of the challenges facing society, from healthcare to sustainable energy. In particular, we model, analyse, design and build biological and biochemical systems in living cells and/or in cell extracts, both exploring and enhancing the engineering potential of biology.

As part of our research we develop novel methods to accelerate the celebrated Design-Build-Test-Learn synthetic biology cycle. As such research in the Centre for Synthetic Biology highly multi- and interdisciplinary covering computational modelling and machine learning approaches; automated platform development and genetic circuit engineering ; multi-cellular and multi-organismal interactions, including gene drive and genome engineering; metabolic engineering; in vitro/cell-free synthetic biology; engineered phages and directed evolution; and biomimetics, biomaterials and biological engineering.

Publications

Citation

BibTex format

@article{Jonas:2018:10.1016/j.synbio.2018.01.001,
author = {Jonas, FRH and Royle, KE and Aw, R and Stan, G and Polizzi, KM},
doi = {10.1016/j.synbio.2018.01.001},
journal = {Synthetic and Systems Biotechnology},
pages = {64--75},
title = {Investigating the consequences of asymmetric endoplasmic reticulum inheritance in Saccharomyces cerevisiae under stress using a combination of single cell measurements and mathematical modelling},
url = {http://dx.doi.org/10.1016/j.synbio.2018.01.001},
volume = {3},
year = {2018}
}

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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Adaptation allows organisms to maintain a constant internal environment, which is optimised for growth. The unfolded protein response (UPR) is an example of a feedback loop that maintains endoplasmic reticulum (ER) homeostasis, and is characteristic of how adaptation is often mediated by transcriptional networks. The more recent discovery of asymmetric division in maintaining ER homeostasis, however, is an example of how alternative non-transcriptional pathways can exist, but are overlooked by gold standard transcriptomic or proteomic population-based assays. In this study, we have used a combination of fluorescent reporters, flow cytometry and mathematical modelling to explore the relative roles of asymmetric cell division and the UPR in maintaining ER homeostasis. Under low ER stress, asymmetric division leaves daughter cells with an ER deficiency, necessitating activation of the UPR and prolonged cell cycle during which they can recover ER functionality before growth. Mathematical analysis of and simulation results from our mathematical model reinforce the experimental observations that low ER stress primarily impacts the growth rate of the daughter cells. These results demonstrate the interplay between homeostatic pathways and the importance of exploring sub-population dynamics to understand population adaptation to quantitatively different stresses.
AU  - Jonas,FRH
AU  - Royle,KE
AU  - Aw,R
AU  - Stan,G
AU  - Polizzi,KM
DO  - 10.1016/j.synbio.2018.01.001
EP  - 75
PY  - 2018///
SN  - 2405-805X
SP  - 64
TI  - Investigating the consequences of asymmetric endoplasmic reticulum inheritance in Saccharomyces cerevisiae under stress using a combination of single cell measurements and mathematical modelling
T2  - Synthetic and Systems Biotechnology
UR  - http://dx.doi.org/10.1016/j.synbio.2018.01.001
UR  - http://hdl.handle.net/10044/1/56668
VL  - 3
ER  -