Conversion of a gene-specific repressor to a regional silencer

Genes & Development
Laura N Rusche, J Rine

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.

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Citations

Mar 17, 2004·Biochimica Et Biophysica Acta·Michael WeinreichCatherine A Fox
Mar 28, 2002·Current Opinion in Genetics & Development·Roger D Kornberg, Yahli Lorch
Aug 23, 2011·The Journal of Biological Chemistry·April L MacKellar, Arno L Greenleaf
Jul 23, 2002·Molecular Biology of the Cell·Laura N RuschéJasper Rine
Oct 19, 2004·Genes & Development·Jennifer E G GallagherSusan J Baserga
Oct 29, 2008·Molecular and Cellular Biology·Patrick J Lynch, Laura N Rusche
Feb 9, 2011·Molecular and Cellular Biology·Brian GelfandAndrew K Vershon
Jan 24, 2007·Molecular and Cellular Biology·Janet MeadAndrew K Vershon
Feb 13, 2008·Molecular and Cellular Biology·Alexias SafiLaura N Rusche
Jun 22, 2011·Molecular and Cellular Biology·Cara A Froyd, Laura N Rusche
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