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Title:Strategies for the production and release of colicin E2 in E. Coli
Author(s):Roychowdhury, Sayan
Contributor(s):Lu, Ting
Degree:B.S. (bachelor's)
Subject(s):biological systems modeling
systems biology
SOS system
stress response
Abstract:Bacterial competition is often driven by the production and release of bacteriocin. Colicins, one class of bacteriocins in Escherichia coli, are protein antibiotics against closely related, competing strains. Colicins exert their bactericidal activity through two major modes of action: membrane pore formation and inhibition of macromolecular synthesis. It has been discovered that colicins are only released through cell lysis, meaning that cells kill competitors at a cost to their own population growth. Although interesting, this topic is largely unexplored: the underlying mechanism controlling the timing of suicide and the trade-off in maximizing colicin production and release remain unclear. We hypothesize that the timing of this decision is made at the single-cell level in the gene network of colicin production, which adds up to the population-level response. To test this hypothesis, we choose colicin E2 as an example and build a model to describe its dynamic responses in terms of colicin production and release in a changing environment. External stressors trigger a SOS response in E. coli carrying the colE2 operon, leading to differential expressions of three genes: (1) the activity gene which encodes the toxin, (2) the immunity gene which protects the host E. coli from being killed by the toxin, and (3) the lysis gene which elicits cell lysis and the subsequent colicin release. With this model, we could explain the strategy cells employ to control colicin production and release and how timing characteristics propagate from single-cell to population level. The stress response of this type can be biologically significant since it boosts our understanding of cell survival strategy in bacterial competition.
Issue Date:2016-05
Genre:Dissertation / Thesis
Date Available in IDEALS:2016-08-30

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