Affiliation:
1. Institut de Recherche en Biologie Moléculaire, Centre National de la Recherche Scientifique, 75221 Paris Cedex 05, France
Abstract
In
Escherichia coli
, expression of the
tif-1
mutation (in the
recA
gene) induces the “SOS response” at 40°C, including massive synthesis of the
recA
(
tif
) protein, cell filamentation, appearance of new repair and mutagenic activities, and prophage induction. Expression of the
tsl-1
mutation (in the
lexA
gene) induces massive synthesis of the
recA
protein and cell filamentation at 42°C, although other SOS functions are not induced. In this paper we show that the septation inhibition induced in
tif
and
tsl
strains at 42°C is not due to the presence of a high concentration of
recA
protein since (i) no
recA
mutants (≤10
−8
) were isolated among thermoresistant nonfilamenting revertants of a
tif-1 tsl-1
strain, (ii) in a
tsl-1 zab-53
strain, only the low basal level of
recA
protein was synthesized at 42°C, yet cell division was inhibited, and (iii) in a
tsl-1 recA99
(amber) strain, no
recA
protein could be detected at 42°C, yet cell division was inhibited. Among suppressors of
tsl-tif
-induced lethality are mutations at a locus which we call
infB
, located in the 66- to 83-min region. The
infB1
mutation confers a highly pleiotropic phenotype, which is suggestive of a regulatory defect; it suppressed
tsl-tif
-induced filamentation but not
recA
protein synthesis, it did not suppress ultraviolet-induced filamentation (in a
lon
derivative), and it reduced but did not abolish
tif
-mediated induction of λ prophage and bacterial mutagenesis. The dissociation of
tsl-tif
-induced septation inhibition and
recA
protein synthesis in the
tif-1 tsl-1 infB1
strain suggests that the control of SOS filamentation may not be strictly identical to the control of
recA
protein synthesis.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
19 articles.
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