Abstract
BackgroundCell division in Bacillus subtilis occurs precisely at midcell. Positional control of cell division is exerted by two mechanisms: nucleoid occlusion, through Noc, which prevents division through nucleoids, and the Min system, where the combined action of the MinC, D and J proteins prevents formation of the FtsZ ring at cell poles or recently completed division sites.Methodology/Principal FindingsWe used a genetic screen to identify mutations in ftsZ that confer resistance to the lethal overexpression of the MinC/MinD division inhibitor. The FtsZ mutants were purified and found to polymerize to a similar or lesser extent as wild type FtsZ, and all mutants displayed reduced GTP hydrolysis activity indicative of a reduced polymerization turnover. We found that even though the mutations conferred in vivo resistance to MinC/D, the purified FtsZ mutants did not display strong resistance to MinC in vitro.Conclusions/SignificanceOur results show that in B. subtilis, overproduction of MinC can be countered by mutations that alter FtsZ polymerization dynamics. Even though it would be very likely that the FtsZ mutants found depend on other Z-ring stabilizing proteins such as ZapA, FtsA or SepF, we found this not to be the case. This indicates that the cell division process in B. subtilis is extremely robust.
Highlights
Rod shaped bacteria divide precisely in the middle by forming a septum to produce two daughter cells
We developed a screen for ftsZ mutants that confer insensitivity to MinC
In which the retention of GFP-MinC/ MinD overexpression was confirmed by checking for the presence of GFP-MinC, and correct integration of the ftsZ mutants in the chromosome was confirmed by a backcross experiment, three ftsZ mutants remained that allowed growth in the presence of elevated MinC/MinD
Summary
Rod shaped bacteria divide precisely in the middle by forming a septum to produce two daughter cells. Nucleoid occlusion is mediated by the DNA binding proteins Noc in Bacillus subtilis [3] and SlmA in Escherichia coli [4]. These proteins become essential in bacteria in which the Min system is knocked out, but as yet their mode of action is unknown [3,4]. Positional control of cell division is exerted by two mechanisms: nucleoid occlusion, through Noc, which prevents division through nucleoids, and the Min system, where the combined action of the MinC, D and J proteins prevents formation of the FtsZ ring at cell poles or recently completed division sites
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