期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 25, 期 14, 页码 6140-6153出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.25.14.6140-6153.2005
关键词
-
资金
- NCI NIH HHS [P01 CA082834, CA82834] Funding Source: Medline
- NIDDK NIH HHS [P30 DK032520, P30 DK32520] Funding Source: Medline
- NIGMS NIH HHS [GM32010, R01 GM032010, GM54137, R01 GM054137] Funding Source: Medline
Genome replication in eukaryotic cells necessitates the stringent coupling of histone biosynthesis with the onset of DNA replication at the G(1)/S phase transition. A fundamental question is the mechanism that links the restriction (R) point late in G, with histone gene expression at the onset of S phase. Here we demonstrate that HiNF-P, a transcriptional regulator of replication-dependent histone H4 genes, interacts directly with p220(NPAT), a substrate of cyclin E/CDK2, to coactivate histone genes during S phase. HiNF-P and p220 are targeted to, and colocalize at, sulmuclear foci (Cajal bodies) in a cell cycle-dependent manner. Genetic or biochemical disruption of the HiNF-P/p220 interaction compromises histone H4 gene activation at the G(1)/S phase transition and impedes cell cycle progression. Our results show that HiNF-P and p220 form a critical regulatory module that directly links histone H4 gene expression at the G(1)/S phase transition to the cyclin E/CDK2 signaling pathway at the R point.
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