Short talk #1: On survival and gene expression during E. coli starvation

Thomas Julou, U. Basel

It is widely believed that bacteria spend most of their life in a non-growing state. However, despite major clinical and ecological implications, very little is known about what controls survival and what determines bacterial phenotypes and survival during starvation. In this talk, I will provide an overview of two recent studies. First, we show that, like the growth rate, the mortality rate during carbon starvation depends critically on subtle differences in environmental conditions. Second, we found that phenotypes are shaped early on upon entry into starvation and last during several days. For this, using a newly designed microfluidic device in combination with fluorescence time-lapse microscopy and automated image analysis, we measured gene expression during starvation by quantifying volumic production of proteins across time in single cells. By combining the observed time-dependent protein production and independently measured degradation rates, we show how protein concentrations deep into stationary phase are determined mainly by the expression dynamics in the first 10 hours of starvation. Finally, using perturbation experiments in which gene expression is inhibited for different periods, we also established that both survival and tolerance to stress during starvation depend strongly on this early expression program. These results contribute to building a quantitative framework for bacterial physiology during starvation.

Short talk #2: Proteome remodeling in starving bacteria

Terry Hwa, UC San Diego

Synthesis of stress proteins is crucial for the survival of starving bacteria. To study processes sustaining gene expression during starvation, we systematically quantified resource allocation in carbon-starved E. coli cells in stationary phase before the onset of cell death. Extensive proteolysis is found to be the primary process fueling protein synthesis and energy biogenesis in starving cells. This starvation-induced protein degradation (SPD), analogous to autophagy in eukaryotes, is surprisingly inefficient, non-specifically targeting a vast number of cytoplasmic proteins including those newly synthesized after entering starvation. Yet, SPD substantially prolongs cell survival, accounting for a major share of viability gain afforded by the RpoS regulon during starvation. We characterize factors turning on and off SPD during starvation, and describe the resulting tradeoff between prolonging survival and maintaining metabolic activities during starvation.

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