Bacterial filaments recover by successive and accelerated asymmetric divisions that allow rapid post-stress cell proliferation

Filamentation is a reversible morphological change triggered in response to various stresses that bacteria might encounter in the environment, during host infection or antibiotic treatments. Here we re-visit the dynamics of filament formation and recovery using a consistent framework based on live-cells microscopy. We compare the fate of filamentous Escherichia coli induced by cephalexin that inhibits cell division or by UV-induced DNA-damage that additionally perturbs chromosome segregation. We show that both filament types recover by successive and accelerated rounds of divisions that preferentially occur at the filaments' tip, thus resulting in the rapid production of multiple daughter cells with tightly regulated size. The DNA content, viability and further division of the daughter cells essentially depends on the coordination between chromosome segregation and division within the mother filament. Septum positioning at the filaments' tip depends on the Min system, while the nucleoid occlusion protein SlmA regulates the timing of division to prevent septum closure on unsegregated chromosomes. Our results not only recapitulate earlier conclusions but provide a higher level of detail regarding filaments division and the fate of the daughter cells. Together with previous reports, this work uncovers how filamentation recovery allows for a rapid cell proliferation after stress treatment.

Automated summary

Filamentation is a reversible morphological change in bacteria triggered by stresses, and this study investigates the dynamics of filament formation and recovery. The results show that both types of filaments, induced by cephalexin or UV-induced DNA-damage, recover through accelerated rounds of divisions at the filaments' tip, resulting in the rapid production of daughter cells with regulated size. The coordination between chromosome segregation and division within the mother filament is crucial for the DNA content, viability, and further division of the daughter cells.