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Global loss of Set1-mediated H3 Lys4 trimethylation is associated with silencing defects in Saccharomyces cerevisiae
被引:83
作者:
Fingerman, IM
Wu, CL
Wilson, BD
Briggs, SD
机构:
[1] Purdue Univ, Dept Biochem, W Lafayette, IN 47907 USA
[2] Purdue Univ, Ctr Canc, W Lafayette, IN 47907 USA
[3] Walther Canc Inst, Indianapolis, IN 46202 USA
关键词:
D O I:
10.1074/jbc.C500097200
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Post-translational histone modifications, such as acetylation, phosphorylation, ubiquitination, and methylation, have been correlated with regulation of gene expression. In Saccharomyces cerevisiae, Set1 has been identified as the sole histone methyltransferase required for histone H3 lysine 4 ( Lys(4)) methylation. Yeast cells that do not express Set1 have several apparent phenotypes, including slow growth and defects in telomere, HML, and rDNA silencing. However, the mechanism by which the Set1 methyltransferase mediates differential histone H3 methylation ( mono-, di-, and tri-) is still not understood, and the involvement of domains or regions in Set1 contributing to H3 Lys(4) methylation has not been well characterized. In this study, the N terminus of Set1 was shown to be important for global and gene specific histone H3 trimethylation. We show that Set1 trimethyl-defective mutants can rescue a set1 Delta slow growth defect. In contrast, Set1 trimethyl mutants were defective in telomere, rDNA, HML, and HMR silencing. Taken together, these data suggest that histone H3 Lys4 trimethylation is required for proper silencing, while mono- and/or dimethylation is sufficient for cell growth.
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页码:28761 / 28765
页数:5
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