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HiNF-P directly links the cyclin E/CDK2/p220NPAT pathway to histone H4 gene regulation at the G1/S phase cell cycle transition.

http://www.ncbi.nlm.nih.gov/pubmed/15988025

Genome replication in eukaryotic cells necessitates the stringent coupling of histone biosynthesis with the onset of DNA replication at the G1/S phase transition. A fundamental question is the mechanism that links the restriction (R) point late in G1 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, subnuclear 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 G1/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 G1/S phase transition to the cyclin E/CDK2 signaling pathway at the R point.

Pubmed ID: 15988025 RIS Download

Mesh terms: Amino Acid Motifs | Animals | CDC2-CDC28 Kinases | Cell Cycle Proteins | Cell Nucleus | Chromatin | Cyclin E | Cyclin-Dependent Kinase 2 | G1 Phase | Gene Expression Regulation | Histones | Humans | Mutation | Nuclear Proteins | Promoter Regions, Genetic | Protein Interaction Mapping | Repressor Proteins | S Phase | Transcription, Genetic | Transcriptional Activation

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Associated grants

  • Agency: NCI NIH HHS, Id: CA82834
  • Agency: NIGMS NIH HHS, Id: GM32010
  • Agency: NIGMS NIH HHS, Id: GM54137
  • Agency: NIDDK NIH HHS, Id: P30 DK32520

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