Regulation of cell division in Escherichia coli: properties of new ftsZ mutants

Abstract

Cells of Escherichia coli which produce high levels of the sfiA protein are UV-sensitive and filament extensively. It has been postulated that the sfiA protein is a division inhibitor which interacts with the ftsZ protein (formerly called sfiB or sulB) leading to cell division arrest. Under certain conditions, a similar division inhibition is observed with cells harboring a mutationally altered tsM allele, another division gene which was postulated to code for a division inhibitor or a controlling effector thereof (Drapeau et al. (1984). In this communication, we report on the properties of ftsZ mutants isolated under conditions which brought no selective pressure. These mutants have either an increased sensitivity to UV irradiation or filament drastically following a nutritional shift-up, or both, or even cannot grow in a rich medium. They presumably possess a ftsZ protein which responds more readily to the inhibitory action of the wild type sfiA or the mutationally altered tsM1 protein since the phenotypic expressions associated with the mutations are not observed in the presence of the sfiA11 mutation or are amplified when the ftsZ mutant cells harbor the tsM1 allele. These results further support earlier suggestions that sfiA modulates ftsZ activity and establish tsM as an additional regulatory element thereof. In addition, it is shown that E. coli strain B is a naturally occurring ftsZ mutant.

The Escherichia coli cell division mutation ftsM1 is in serU

“…Previous studies in our laboratory revealed that when the well-known cell division mutation ftsZ84 was introduced into ftsMl mutant cells, these cells grew as filaments on minimal medium but failed to form colonies on rich medium, whereas cells bearing either one of the two mutations grew well on both media. It was postulated that this incapacity to grow on rich media was due to the accentuation of the division defect of ftsZ84 by ftsMl, possibly through interactions of their gene products (4). However, since the ftsMI phenotypes now appear to be due to the action of a suppressor tRNA, such hypothetical interactions are not essential; the amplified division defect could simply result from the synthesis of a faulty FtsZ84 protein by ftsMl.…”

“…Plasmid pBH15 is a pBR325 derivative containing the ftsZ+ gene, and its construction has been reported previously (4). pPHB3 is a low-copy-number plasmid with the pSC101 origin of replication and containing theftsZ+ gene.…”

Identification of three cytotoxic early proteins of mycobacteriophage L5 leading to growth inhibition in Mycobacterium smegmatis

“…These proteins form a structure called Z-ring, a cytoskeletal scaffold mediating cell division (Datta et al, 2006). Alteration of Z-ring proteins also leads to growth inhibition and impaired cell division in both E. coli and M. smegmatis (Belhumeur & Drapeau, 1984;Dziadek et al, 2003). Furthermore, simultaneous deletion of several lowmolecular-mass PBPs of E. coli leads to elongation and branching of individual mutants (Nelson & Young, 2000).…”

Unusual observations during construction of a new cloning vector providing lon gene expression in Escherichia coli

“…Another function of lon is seen in cell division, in which lon controls the half-life of the cell division inhibitor SulA (Belhumeur and Drapeau, 1984). E. coli Ion mutants exhibit an increased stability of SulA, thus inhibiting cell division by inhibiting FtsZ, an essential cell division protein (Lutkenhaus et al, 1986).…”