Yeast and mammalian Sin3-Rpd3 histone deacetylase complexes function as transcriptional
repressors when recruited by promoter-specific transcription factors.
Based on sequence similarity to human SAP30, we have identified Sap30 as
a novel component of a yeast Sin3-Rpd3 complex. The SAP30 gene is
not essential for cell viability, but sap30 mutants exhibit
phenotypes comparable to sin3 and rpd3 mutants, including
cycloheximide-sensitivity, mating and sporulation defects, and gene-specific transcriptional derepression. Consistent with its role as a
transcriptional repressor, a LexA-Sap30 fusion protein repressed
transcription of a LexA op -lacZ reporter. It was shown
previously that sin3 and rpd3 deletions enhance silencing
at the HMR locus and that rpd3 enhances the telomere
position effect. Here we confirm and extend those results by showing
that Rpd3, Sin3 and Sap30 are required to overcome genomic silencing at
telomeres and the HMR locus. Furthermore, these effects are
dependent upon Rpd3 histone deacetylase activity. Enhanced silencing
associated with disruption of the Sin3-Rpd3 complex is partially
suppressed by disruption of CAC3/MSI1 , which encodes a subunit of
the CAF-1 chromatin assembly factor, and by disruption of the
GCN5 -encoded histone acetyltransferase. These results define
Sap30 as a novel component of the Sin3-Rpd3 complex that functions in
both transcriptional repression and in counteracting genomic
silencing.
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