期刊
NUCLEIC ACIDS RESEARCH
卷 46, 期 3, 页码 1331-1344出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkx1276
关键词
-
资金
- NCI [R01 CA198482, T32 CA009156]
- V Foundation Translational Science Award
- Lineberger Comprehensive Cancer Center/FACS facility - CCSG [P30 CA016086]
- NIH [R01GM68088]
- Cancer Center Core Support Grant [P30 CA016086]
Methylation of histone H3 lysine 36 ( H3K36me) by yeast Set2 is critical for the maintenance of chromatin structure and transcriptional fidelity. However, we do not know the full range of Set2/H3K36me functions or the scope of mechanisms that regulate Set2-dependent H3K36 methylation. Here, we show that the APC/C-CDC20 complex regulates Set2 protein abundance during the cell cycle. Significantly, absence of Set2-mediated H3K36me causes a loss of cell cycle control and pronounced defects in the transcriptional fidelity of cell cycle regulatory genes, a class of genes that are generally long, hence highly dependent on Set2/H3K36me for their transcriptional fidelity. Because APC/C also controls human SETD2, and SETD2 likewise regulates cell cycle progression, our data imply an evolutionarily conserved cell cycle function for Set2/SETD2 that may explain why recurrent mutations of SETD2 contribute to human disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据