MraZ Transcriptionally Controls the Critical Level of FtsL Required for Focusing Z-Rings and Kickstarting Septation in Bacillus subtilis

Autor: Maria L. White, Abigail Hough-Neidig, Sebastian J. Khan, Prahathees J. Eswara
Rok vydání: 2022
Předmět:
Zdroj: J Bacteriol
ISSN: 1098-5530
0021-9193
Popis: The bacterial division and cell wall (idcw/i) cluster is a highly conserved region of the genome which encodes several essential cell division factors, including the central divisome protein FtsZ. Understanding the regulation of this region is key to our overall understanding of the division process.imraZ/iis found at the 5' end of theidcw/icluster, and previous studies have described MraZ as a sequence-specific DNA binding protein. In this article, we investigate MraZ to elucidate its role in Bacillus subtilis. Through our investigation, we demonstrate that increased levels of MraZ result in lethal filamentation due to repression of its own operon (imraZ/i-imraW/i-iftsL/i-ipbpB/i). We observed rescue of filamentation upon decouplingiftsL/iexpression, but not other genes in the operon, from MraZ control. Our data suggest that regulation of theimra/ioperon may be an alternative way for cells to quickly arrest cytokinesis, potentially during entry into the stationary phase and in the event of DNA replication arrest. Furthermore, through time-lapse microscopy, we were able to identify that overexpression ofimraZ/ior depletion of FtsL results in decondensation of the FtsZ ring (Z-ring). Using fluorescent d-amino acid labeling, we also observed that coordinated peptidoglycan insertion at the division site is dysregulated in the absence of FtsL. Thus, we reveal that the precise role of FtsL is in Z-ring maturation and focusing septal peptidoglycan synthesis.bIMPORTANCE/bMraZ is a highly conserved protein found in a diverse range of bacteria, including genome-reducediMycoplasma/i. We investigated the role of MraZ in Bacillus subtilis and found that overproduction of MraZ is toxic due to cell division inhibition. Upon further analysis, we observed that MraZ is a repressor of its own operon, which includes genes that encode the essential cell division factors FtsL and PBP2B. We noted that decoupling ofiftsL/ialone was sufficient to abolish MraZ-mediated cell division inhibition. Using time-lapse microscopy, we showed that under conditions where the FtsL level is depleted, the cell division machinery is unable to initiate cytokinesis. Thus, our results pinpoint that the precise role of FtsL is in concentrating septal cell wall synthesis to facilitate cell division.
Databáze: OpenAIRE
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