Abstract:
:In Saccharomyces cerevisiae, gene silencing at the HMR and HML loci is normally dependent on Sir2p, Sir3p, and Sir4p, which are structural components of silenced chromatin. Sir2p is a NAD+-dependent histone deacetylase required for silencing. Silencing can be restored in cells lacking Sir proteins by a dominant mutation in SUM1, which normally acts as a mitotic repressor of meiotic genes. This study found that mutant Sum1-1p, but not wild-type Sum1p, associated directly with HM loci. The origin recognition complex (ORC) was required for Sum1-1p-mediated silencing, and mutations in ORC genes reduced association of Sum1-1p with the HM loci. Sum1-1p-mediated silencing also depended on HST1, a paralog of SIR2. Both Sum1-1p and wild-type Sum1p interacted with Hst1p in coimmunoprecipitation experiments. Therefore, the SUM1-1 mutation did not change the affinity of Sum1p for Hst1p, but rather relocalized Sum1p to the HM loci. Sum1-1-Hst1p action led to hypoacetylation of the nucleosomes at HM loci. Thus, Sum1-1p and Hst1p could substitute for Sir proteins to achieve silencing through formation of a compositionally distinct type of heterochromatin.
journal_name
Genes Devjournal_title
Genes & developmentauthors
Rusché LN,Rine Jdoi
10.1101/gad.873601subject
Has Abstractpub_date
2001-04-15 00:00:00pages
955-67issue
8eissn
0890-9369issn
1549-5477journal_volume
15pub_type
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pub_type: 杂志文章
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更新日期:2008-11-01 00:00:00
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journal_title:Genes & development
pub_type: 杂志文章
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更新日期:2008-06-01 00:00:00
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