Person:
Mukherjee, Avik

Loading...
Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Mukherjee

First Name

Avik

Name

Mukherjee, Avik

Search Results

Now showing 1 - 2 of 2
  • Publication
    Survival dynamics of starving bacteria are determined by ion homeostasis that maintains plasmolysis
    (Springer Science and Business Media LLC, 2024-05-23) Schink, Severin; Polk, Marku; Athaide, Edward; Mukherjee, Avik; Ammar, Constantin; Liu, Xili; Oh, Seungeun; Chang, Yu-Fang; Basan, Markus
    The ability to survive starvation is an integral part of bacterial fitness and determines composition, turn-over and biodiversity in microbial ecosystems. Starving bacteria enter a state, in which their cytoplasm is contracted from the cell wall, known as plasmolysis. Plasmolysis is often thought to be a pathological, passive condition, arising automatically from the lack of ATP. Here, we show that contrary to this existing notion, maintaining plasmolysis is an active, ATP-consuming state that is essential for starvation survival. We show that ion homeostasis for maintaining plasmolysis consumes the lion’s share of starving cells’ energy budget and directly determines death rates in starvation. A quantitative mathematical model accurately predicts death rates across diverse starvation conditions and perturbations. This enabled the development of an optimized starvation medium that would be ideally suited for preserving and transplanting natural microbial communities by maintaining viability but preventing outgrowth of a subset of species.
  • Publication
    A Universal Trade-Off Between Growth and Lag in Fluctuating Environments
    (Springer Science and Business Media LLC, 2020-07-15) Basan, Markus; Honda, Tomoya; Christodoulou, Dimitris; Hörl, Manuel; Chang, Yu Fang; Leoncini, Emanuele; Mukherjee, Avik; Okano, Hiroyuki; Taylor, Brian R.; Silverman, Josh M.; Sanchez, Carlos; Williamson, James R.; Paulsson, Johan; Hwa, Terence; Sauer, Uwe
    The rate of cell growth is widely recognized as crucial for fitness in bacteria1,2 and a main driver of proteome allocation, but it is unclear how growth rates are ultimately determined. Increasing evidence suggests that other objectives also play key roles3–7, such as the rate of physiological adaption to changing environments8,9. The challenge for cells is that these objectives cannot be independently optimized, and maximizing one may even minimize another. Many such tradeoffs have indeed been hypothesized, but so far they have mostly been based on qualitative correlative studies8–11, and often lacked mechanistic bases. Here we report the occurrence of a tradeoff between steady-state growth and adaptability for Escherichia coli, upon abruptly shifting a growing culture from a preferred carbon source (e.g., glucose) to fermentation products (e.g., acetate). Such transitions, which are common for enteric bacteria, are often accompanied by multi-hour lags before growth resumes. The inverse lag time for dozens of shifts was found to quantitatively exhibit the same linear dependence on pre-shift growth rates, approaching zero (infinite lag) at the maximum growth rate. Metabolomic analysis revealed that the long lags resulted from the depletion of key metabolites due to the sudden reversal of central carbon flux imposed by these nutrient shifts. The metabolic data led us to a model of sequential flux limitation which not only explained the observed universal tradeoff between growth and adaptability, but also generated other quantitative predictions that then could be validated experimentally. This shows that the trade-off reflects the opposing enzyme requirements for effective glycolysis versus gluconeogenesis.