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J. Bacteriol., Mar 1997, 1931-1939, Vol 179, No. 6
TM Hill, B Sharma, M Valjavec-Gratian and J Smith
In Escherichia coli, damage to DNA induces the expression of a set of genes
known collectively as the SOS response. Part of the SOS response includes
genes that repair DNA damage, but another part of the response coordinates
DNA replication and septation to prevent untimely cell division. The
classic SOS gene product that inhibits cell division is SfiA (or SulA),
which binds to FtsZ and prevents septum formation until the DNA damage has
been repaired. However, another pathway acts to coordinate DNA replication
and cell division when sfiA, or the sfi- dependent pathway, is inoperative.
Until recently, little was known of this alternative pathway, which is
called the sfi-independent pathway. We report here that sfi-independent
filamentation is suppressed by lexA(Ind-) mutations, suggesting that
derepression of the LexA regulon is necessary for sfi-independent
induction. However, expression of LexA- controlled genes is not sufficient;
DNA damage is also required to induce this secondary pathway of cell
division inhibition. Furthermore, we postulate that loss of the common
regulatory circuitry of the sfi- dependent and sfi-independent pathways by
recA or lexA mutants uncouples cell division and DNA replication.
Copyright © 1997, American Society for Microbiology
sfi-independent filamentation in Escherichia coli Is lexA dependent and requires DNA damage for induction
Department of Microbiology and Immunology, University of North Dakota School of Medicine, Grand Forks 58202-9037, USA. tomhill@mail.med.und.nodak.edu
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