Affiliation:
1. Departments of Genetics1 and
2. Medicine,2 Stanford University School of Medicine, Stanford, California 94305-5120
Abstract
ABSTRACT
SLP1
int
is a 17.2-kb genetic element that normally is integrated site specifically into the chromosome of
Streptomyces coelicolor
A3(2). The
imp
operon within SLP1
int
represses replication of both chromosomally integrated and extrachromosomal SLP1. During mating with
S. lividans
, SLP1
int
can excise, delete part of
imp
, and form a family of autonomously replicating conjugative plasmids. Earlier work has shown that
impA
and
impC
gene products act in concert to control plasmid maintenance and regulate their own transcription. Here we report that these
imp
genes act also on a second promoter, P
op
imp
(promoter opposite
imp
), located adjacent to, and initiating transcription divergent from,
imp
to regulate loci involved in the intramycelial transfer of SLP1 plasmids.
spdB1
and
spdB2
, two overlapping genes immediately 3′ to P
op
imp
and directly regulated by
imp
, are shown by Tn
5
mutagenesis to control transfer-associated growth inhibition (i.e., pocking). Additional genes resembling transfer genes of other
Streptomyces
spp. plasmids and required for SLP1 transfer and/or postconjugal intramycelial spread are located more distally to P
op
imp
. Expression of
impA
and
impC
in an otherwise competent recipient strain prevented SLP1-mediated gene transfer of chromosomal and plasmid genes but not plasmid-independent chromosome-mobilizing activity, suggesting that information transduced to recipients after the formation of mating pairs affects
imp
activity. Taken together with earlier evidence that the
imp
operon regulates SLP1 DNA replication, the results reported here implicate
imp
in the overall regulation of functions related to the extrachromosomal state of SLP1.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
10 articles.
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