Journal of Bacteriology, November 2000, p. 6203-6213, Vol. 182, No. 21
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Department of Microbiology and Molecular Genetics, University of Texas-Houston Medical School, Houston, Texas 77030
Received 22 May 2000/Accepted 28 July 2000
To investigate the interaction between FtsZ and the Min system
during cell division of Escherichia coli, we examined the
effects of combining a well-known thermosensitive mutation of
ftsZ, ftsZ84, with
minCDE, a
deletion of the entire min locus. Because the Min system is
thought to down-regulate Z-ring assembly, the prediction was that
removing minCDE might at least partially suppress the thermosensitivity of ftsZ84, which can form colonies below
42°C but not at or above 42°C. Contrary to expectations, the double mutant was significantly more thermosensitive than the
ftsZ84 single mutant. When shifted to the new lower
nonpermissive temperature, the double mutant formed long filaments
mostly devoid of Z rings, suggesting a likely cause of the increased
thermosensitivity. Interestingly, even at 22°C, many Z rings were
missing in the double mutant, and the rings that were present were
predominantly at the cell poles. Of these, a large number were present
only at one pole. These cells exhibited a higher than expected
incidence of polar divisions, with a bias toward the newest pole.
Moreover, some cells exhibited dramatically elongated septa that
stained for FtsZ, suggesting that the double mutant is defective in
Z-ring disassembly, and providing a possible mechanism for the polar bias. Thermoresistant suppressors of the double mutant arose that had
modestly increased levels of FtsZ84. These cells also exhibited elongated septa and, in addition, produced a high frequency of branched
cells. A thermoresistant suppressor of the ftsZ84 single mutant also synthesized more FtsZ84 and produced branched cells. The
evidence from this study indicates that removing the Min system exposes
and exacerbates the inherent defects of the FtsZ84 protein, resulting
in clear septation phenotypes even at low growth temperatures. Increasing levels of FtsZ84 can suppress some, but not all, of these phenotypes.
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