Journal of Bacteriology, December 1998, p. 6306-6315, Vol. 180, No. 23
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
State Scientific Research Institute of Genetics and Selection of Industrial Microorganisms, Moscow 113545, Russia,1 and Institut Jacques Monod (Centre National de la Recherche Scientifique, Université Paris 7), 75251 Paris Cedex 05, France2
Received 21 July 1997/Accepted 1 October 1998
Two Escherichia coli genes, expressed from multicopy
plasmids, are shown to cause partial induction of prophage
in
recA mutant lysogens. One is rcsA, which
specifies a positive transcriptional regulator of the cps
genes, which are involved in capsular polysaccharide synthesis. The
other is dsrA, which specifies an 85-nucleotide RNA that
relieves repression of the rcsA gene by histone-like protein H-NS. Genetic contexts known to increase Cps expression also
cause RecA-independent
induction: the rcsC137 mutation, which causes constitutive Cps expression, and the lon and
rcsA3 mutations, which stabilize RcsA. Lambdoid phages 21,
80, and 434 are also induced by RcsA and DsrA overexpression in
recA lysogens. Excess
cI repressor specifically blocks
induction, suggesting that induction involves repressor
inactivation rather than repressor bypass. RcsA-mediated induction
requires RcsB, the known effector of the cps operon,
whereas DsrA-mediated induction is RcsB independent in stationary
phase, pointing to the existence of yet another RecA-independent
pathway of prophage induction.
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