The Escherichia coli minB mutation resembles gyrB in defective nucleoid segregation and decreased negative supercoiling of plasmids.
Nucleoid segregation in the Escherichia coli minB mutant and in cells that over-produce minB gene products appeared defective as measured from fluorescence micrographs. Electrophoretic resolution of topoisomers of plasmid isolates from the minB strain revealed a decreased level of negative supercoiling; in addition, multimerization was observed. Over-production of the minB gene product also resulted in a decreased level of negative supercoiling. This phenotype is typical of the gyrB(ts) mutant, which is known to be affected in chromosome decatenation and supercoiling. We propose that the minB mutation and over-production of the minB gene products cause a defect in nucleoid segregation, which may be related to the decrease in negative supercoiling. As in the gyrB(ts) mutant, retardation of nucleoid segregation is proposed to inhibit constriction initiation in the cell centre and to give rise to nucleoid-free cell poles. As a consequence, these cells divide between nucleoid and cell pole, resulting in minicell and (sometimes) in anucleate cell formation.
Mulder
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E
Department of Molecular Cell Biology, University of Amsterdam, The Netherlands.
El'Bouhali
M
M
Pas
E
E
Woldringh
C L
CL
D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics; D004269:DNA, Bacterial / Q000235:genetics*; D004278:DNA, Superhelical / Q000235:genetics*; D004926:Escherichia coli / Q000235:genetics* / Q000378:metabolism / Q000648:ultrastructure; D008856:Microscopy, Fluorescence; D009154:Mutation; D015388:Organelles / Q000378:metabolism; D010957:Plasmids
D001426:Bacterial Proteins; D004269:DNA, Bacterial; D004278:DNA, Superhelical