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Molecular and Cellular Biology, September 1998, p. 5511-5522, Vol. 18, No. 9
Institute of Microbial Technology, Sector 39 A, Chandigarh
160 036, Punjab, India,1 and
Developmental Genetics Section, Gene Regulation and
Chromosome Biology Laboratory, ABL-Basic Research Program,
NCI-Frederick Cancer Research and Development Center,
Frederick, Maryland 21702-12012
Received 11 February 1998/Returned for modification 31 March
1998/Accepted 15 June 1998
Recent studies have indicated that the DNA replication machinery is
coupled to silencing of mating-type loci in the budding yeast
Saccharomyces cerevisiae, and a similar silencing mechanism may operate in the distantly related yeast Schizosaccharomyces pombe. Regarding gene regulation, an important function of DNA replication may be in coupling of faithful chromatin assembly to
reestablishment of the parental states of gene expression in daughter
cells. We have been interested in isolating mutants that are defective
in this hypothesized coupling. An S. pombe mutant fortuitously isolated from a screen for temperature-sensitive growth
and silencing phenotype exhibited a novel defect in silencing that
was dependent on the switching competence of the mating-type loci, a
property that differentiates this mutant from other silencing mutants
of S. pombe as well as of S. cerevisiae. This unique mutant phenotype defined a locus
which we named sng1 (for silencing not governed). Chromatin
analysis revealed a switching-dependent unfolding of the donor loci
mat2P and mat3M in the
sng1
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
A Novel Function of the DNA Repair Gene rhp6 in
Mating-Type Silencing by Chromatin Remodeling in Fission
Yeast
mutant, as indicated by increased
accessibility to the in vivo-expressed Escherichia coli dam
methylase. Unexpectedly, cloning and sequencing identified
the gene as the previously isolated DNA repair gene rhp6.
RAD6, an rhp6 homolog in S. cerevisiae, is required for postreplication DNA repair and
ubiquitination of histones H2A and H2B. This study implicates the
Rad6/rhp6 protein in gene regulation and, more importantly, suggests
that a transient window of opportunity exists to ensure the remodeling
of chromatin structure during chromosome replication and recombination.
We propose that the effects of the
sng1
/rhp6
mutation on silencing
are indirect consequences of changes in chromatin structure.
*
Corresponding author. Mailing address for Jagmohan
Singh: Institute of Microbial Technology, Sector 39 A, Chandigarh 160 036, Punjab, India. Phone: 91-172-690908, ext. 443. Fax: 91-172-690585 or 91-172-690632. E-mail: Jag{at}koel.imtech.ernet.in. Mailing address for Amar J. S. Klar: NCI-Frederick Cancer Research and
Development Center, ABL-Basic Research Program, Gene Regulation and
Chromosome Biology Laboratory, Developmental Genetics Section, P.O. Box
B, Frederick, MD 21702-1201. Phone: (301) 846-5149. Fax: (301)
846-6911. E-mail: klar{at}ncifcrf.gov.
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