Abstract
AbstractMany bacterial species grow into filaments under stress conditions. Initially regarded as an indicator of cell death, filamentation is now proposed to be a transient morphological change that improves bacterial survival in hostile environments. However, the mechanism of filament recovery remains poorly characterized. Using real-time microscopy in live-cells, we analysed the fate of filamentous Escherichia coli induced by antibiotic-mediated specific inhibition of cell division, or by UV-induced DNA-damage that additionally perturbs chromosome segregation. Both filament types recover by successive and accelerated rounds of divisions, which are preferentially positioned asymmetrically at the tip of the cell by the Min system. Such division dynamics allows the rapid production of daughter cells with normal size, which DNA content depends on the progression of chromosome segregation prior to division. In most filaments, nucleoid segregation precedes tip-division, which produces nucleated daughter cells that resume normal growth. However, when segregation is deficient, tip-division occurs in the absence of DNA and produces anucleated cells. These findings uncover the mechanism by which bacterial filamentation allows efficient post-stress cell proliferation.One Sentence SummaryBacterial filaments recover by successive, frequent and Min-dependent asymmetric tip-divisions that rapidly produce multiple daughter cells with normal size and viability
Publisher
Cold Spring Harbor Laboratory
Cited by
9 articles.
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