Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 25, Issue 14, Pages 6140-6153Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.25.14.6140-6153.2005
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Funding
- 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
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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.
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