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BacFlash signals acid-resistance gene expression in bacteria
Di Wu1, Wenfeng Qi1, Wei Nie1,2
1State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Cell Research
|November 7, 2020
Summary
Bacteria possess a novel acid-resistance mechanism called BacFlash, triggered by proton leaks. This electrochemical excitation primes cells for survival against extreme acid stress by activating key genes.
Area of Science:
- Microbiology
- Cellular Physiology
- Biochemistry
Background:
- Intracellular pH (pHi) homeostasis is vital for cellular functions and bacterial survival, impacting physiology, ecology, and pathogenesis.
- Understanding bacterial acid resistance (AR) mechanisms is crucial for various applications, including medicine and biotechnology.
Purpose of the Study:
- To elucidate a novel bacterial acid-resistance mechanism involving electrochemical excitation.
- To identify the molecular components and triggers of this acid-resistance response.
Main Methods:
- Genome-wide screening to identify genetic components involved in the response.
- Measurement of membrane potential, intracellular pH, and reactive oxygen species production.
- Analysis of gene expression changes under acid stress.
Main Results:
- Discovery of 'BacFlash', a quantal electrochemical excitation involving membrane depolarization, transient pHi rise, and reactive oxygen species burst.
- Identification of proton leak as the trigger for BacFlash, with its frequency inversely correlated to pHi buffering capacity.
- Identification of ATP synthase Fo complex subunit a as a potential proton sensor.
- Demonstration that sustained BacFlash hyperactivity induces AR genes and enhances survival under extreme acid stress.
Conclusions:
- A novel bacterial acid-resistance mechanism, BacFlash, couples electrochemical excitation to gene expression for enhanced survival.
- This mechanism represents a pre-emptive response to acid stress, mediated by proton sensing and leading to transcriptional activation of AR genes.
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