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The Paf1 complex is required for histone H3 methylation by COMPASS and Dot1p: linking transcriptional elongation to histone methylation 总被引:11,自引:0,他引:11
Krogan NJ Dover J Wood A Schneider J Heidt J Boateng MA Dean K Ryan OW Golshani A Johnston M Greenblatt JF Shilatifard A 《Molecular cell》2003,11(3):721-729
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Dehé PM Pamblanco M Luciano P Lebrun R Moinier D Sendra R Verreault A Tordera V Géli V 《Journal of molecular biology》2005,353(3):477-484
The yeast Set1-complex catalyzes histone H3 lysine 4 (H3K4) methylation. Using N-terminal Edman sequencing, we determined that 50% of H3K4 is methylated and consists of roughly equal amounts of mono, di and tri-methylated H3K4. We further show that loss of either Paf1 of the Paf1 elongation complex, or ubiquitination of histone H2B, has only a modest effect on bulk histone mono-methylation at H3K4. Despite the fact that Set1 recruitment decreases in paf1delta cells, loss of Paf1 results in an increase of H3K4 mono-methylation at the 5' coding region of active genes, suggesting a Paf1-independent targeting of Set1. In contrast to Paf1 inactivation, deleting RTF1 affects H3K4 mono-methylation at the 3' coding region of active genes and results in a decrease of global H3K4 mono-methylation. Our results indicate that the requirements for mono-methylation are distinct from those for H3K4 di and tri-methylation, and point to differences among members of the Paf1 complex in the regulation of H3K4 methylation. 相似文献
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The DNA damage checkpoint response requires histone H2B ubiquitination by Rad6-Bre1 and H3 methylation by Dot1 总被引:1,自引:0,他引:1
Giannattasio M Lazzaro F Plevani P Muzi-Falconi M 《The Journal of biological chemistry》2005,280(11):9879-9886
The cellular response to DNA lesions entails the recruitment of several checkpoint and repair factors to damaged DNA, and chromatin modifications may play a role in this process. Here we show that in Saccharomyces cerevisiae epigenetic modification of histones is required for checkpoint activity in response to a variety of genotoxic stresses. We demonstrate that ubiquitination of histone H2B on lysine 123 by the Rad6-Bre1 complex, is necessary for activation of Rad53 kinase and cell cycle arrest. We found a similar requirement for Dot1-dependent methylation of histone H3. Loss of H3-Lys(79) methylation does not affect Mec1 activation, whereas it renders cells checkpoint-defective by preventing phosphorylation of Rad9. Such results suggest that histone modifications may have a role in checkpoint function by modulating the interactions of Rad9 with chromatin and active Mec1 kinase. 相似文献
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Methylation of histone H3 by Set2 in Saccharomyces cerevisiae is linked to transcriptional elongation by RNA polymerase II
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Krogan NJ Kim M Tong A Golshani A Cagney G Canadien V Richards DP Beattie BK Emili A Boone C Shilatifard A Buratowski S Greenblatt J 《Molecular and cellular biology》2003,23(12):4207-4218
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