In Saccharomyces cerevisiae, transcriptional silencing of the cryptic mating loci HML and HMR is established by the combined actions of cis-acting silencers and trans-acting proteins, including Sir2p, Sir3p and Sir4p. The Sir proteins serve as an integral part of a special silent chromatin at the HM loci. Deletion of any of the SIR2-SIR4 genes leads to a complete loss of silencing. However, the SUM1-1 mutation can restore silencing at the HM loci. Recently, it has been shown that Sum1-1p is directed to the silencers and internal regions of the HM loci, and interacts with the Hst1p histone deacetylase that is a paralog of the Sir2p histone deacetylase. Like Sir-dependent silent chromatin, Sum1-1p-dependent chromatin is hypoacetylated. These suggest that Sum1-1p and Hst1p play roles similar to those of the Sir proteins in promoting transcriptional silencing. Here, we examine whether Sum1-1p-dependent chromatin is similar to Sir-dependent silent chromatin, which is characterized by densely and precisely positioned nucleosomes. We demonstrate that Sum1-1p-dependent primary chromatin structure at HMR largely resembles, but is not identical with, Sir-dependent silent chromatin, whereas Sum1-1p-dependent HML chromatin largely resembles, but is not identical with, derepressed chromatin found in a sir- background. This correlates with the previous finding that SUM1-1 restores silencing more efficiently at HMR than at HML. We show also that DNA in Sum1-1p-dependent silent chromatin assumes a distinct topology. Moreover, we present evidence indicating that Sum1-1p can increase the stability of Sir-dependent silent chromatin, thereby providing an explanation for the finding that SUM1-1 enhances HML/HMR silencing in a SIR+ background.

• PMID: 16406069
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Journal Article | Research Support, N.I.H., Extramural

Authors

Yu Q, Elizondo S, Bi X

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