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Biology subjects

Biselli, E.

Publications and source records attributed to Biselli, E..

2 recordsLinked to original sources

A quantitative framework for bacterial competition during starvation

Bacterial communities often spend long periods under starvation, where survival depends not only on their intrinsic ability to withstand stress but also on nutrients released by dying neighbors. This creates a distinct form of competition: cells compete for recycled necromass, and the outcome should depend on physiological traits that determine nutrient uptake and maintenance demand. Here, we develop a quantitative framework for this competition using Escherichia coli populations whose starvation physiology is tuned by prior growth history. Fast-grown populations have higher maintenance demands and die slightly faster in monoculture, whereas slow-grown populations are better adapted to starvation. In co-culture, these physiological differences are strongly amplified in a frequency-dependent manner: less-adapted populations die several-fold faster than in monoculture, whereas well-adapted populations can reduce their death rate below that of stationary-phase adapted monocultures. We explain these dynamics with a shared-energy-pool model in which death releases recyclable nutrients, surviving cells consume them for maintenance, and intracellular energy sets death rate. Using independently measured parameters, the model makes parameter-free predictions for competitive survival. The predicted instantaneous death rates collapse onto a universal function of the population ratio over four orders of magnitude. Our results establish necromass recycling as a quantitative basis for bacterial competition during starvation and lay the foundation for modeling communities during starvation.

systems biology↗

A thermal fuse in methionine biosynthesis arrests growth and protects Escherichia coli at elevated temperatures

Adaptive stress resistance in microbes is mostly attributed to the expression of stress response genes, such as heat shock proteins, which prevent deterioration of cellular material. Here, we report a novel response of E. coli to heat stress: induction of a growth-arrested state, caused by degradation of an enzyme in the methionine biosynthesis pathway (MetA). While MetA degradation is detrimental for proliferation, we show that the resulting growth arrest has a direct benefit for survival at high temperatures; it protects cells when temperatures rise beyond 50{degrees}C, increasing the survival chances by over 1000-fold. Using a combination of experiments and mathematical modelling, we show that degradation of MetA leads to the coexistence of growing and non-growing cells, allowing microbes to bet-hedge between continued growth if conditions remain bearable and survival if conditions worsen. We test our model experimentally and verify quantitatively how protein expression, degradation rates and environmental stresses affect the partitioning between growing and non-growing cells. Because growth arrest can be abolished with simple mutations, such as point mutations of MetA and knock-outs of proteases, we interpret the breakdown of methionine synthesis as a system that has evolved to disintegrate at high temperature and shut off growth, analogous to thermal fuses used in engineering to shut off electricity when the device could be damaged by overheating.

microbiology↗