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After 30 Years of Study, the Bacterial SOS Response Still Surprises Us 英文参考文献
Open access, freely available online
Primer
After 30 Years of Study, the Bacterial
SOS Response Still Surprises Us
Bénédicte Michel
I
n order to survive in various environmental conditions,
cells have a repertoire of genes that they can choose
to express or silence according to their needs. Among
this vast collection of genetically controlled networks, the
SOS response is an inducible DNA repair system that allows
bacteria to survive sudden increases in DNA damage. The
importance of the SOS response is underscored by the
observation that this regulatory network is widely present in
bacteria, reflecting the need for all living cells to maintain the
integrity of their genome.
Jump-Starting DNA Repair
The first experimental support for the existence of an
inducible DNA repair network in Escherichia coli was found
30 years ago by Miroslav Radman, who introduced the term
“SOS response” to describe this network [1]. Two proteins
play key roles in the regulation of the SOS response: a
repressor named LexA and an inducer, the RecA filament.
During normal growth, the LexA repressor binds to a specific
sequence—the SOS box, present in the promoter region
of SOS genes—and prevents their expression. SOS genes
are repressed to different degrees under normal growth
conditions. This depends on the exact sequence of their SOS
box (the region of a promoter that is recognized by LexA),
its position in the promoter region, and the strength of the
promoter.
When the cell senses the presence of an increased level
of DNA damage, the LexA repressor undergoes a self-
cleavage reaction and the SOS genes are de-repressed
(Figure 1). A nucleoprotein complex—the RecA filament—
induces the LexA cleavage reaction. RecA is a ubiquitous
protein, present in nearly all bacteria and conserved in all
organisms, including humans. It specifically binds single-
stranded DNA (ssDNA), forming a nucleoprotein filament
that has two functions [2]: the RecA filament may either
invade a homologous double-
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