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    HiNF-D (CDP-cut/CDC2/cyclin A/pRB-complex) influences the timing of IRF-2-dependent cell cycle activation of human histone H4 gene transcription at the G1/S phase transition

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    Authors
    Aziz, Farah
    Van Wijnen, Andre J.
    Stein, Janet L.
    Stein, Gary S.
    UMass Chan Affiliations
    Department of Cell Biology
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    1998-11-10
    Keywords
    Base Sequence; Binding Sites; Cell Cycle; Choline O-Acetyltransferase; DNA-Binding Proteins; G1 Phase; Histones; Humans; Interferon Regulatory Factor-2; Molecular Sequence Data; Mutation; Promoter Regions (Genetics); RNA, Messenger; *Repressor Proteins; S Phase; Time Factors; Transcription Factors; Transcription, Genetic
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    https://doi.org/10.1002/(SICI)1097-4652(199812)177:3<453::AID-JCP8>3.0.CO;2-F
    Abstract
    Cell cycle control of histone H4 gene transcription is mediated by the multipartite promoter domain H4-Site II, which supports transcriptional activation at the G1/S phase transition and modulates basal H4 gene transcription. Proliferation-specific transcription is determined by the integrated activities of three distinct promoter factors interacting with H4-Site II: the interferon regulatory factor IRF-2 (synonymous with HiNF-M), HiNF-D (a complex between the homeodomain protein CDP-cut and the cell cycle mediators CDC2, cyclin A and pRB), as well as HiNF-P/H4TF-2. However, the contribution of HiNF-D to the enhancement and/or suppression of H4 gene transcription at specific cell cycle stages remains to be established. We used a panel of synchronized HeLa S3 cell lines containing stably integrated H4 promoter/CAT reporter gene constructs with mutations in H4-Site II. The temporal regulation of CAT mRNA accumulation under the control of the H4 promoter was analyzed by RNase protection analysis. Our main finding is that mutation of the HiNF-D/CDP-cut binding site alters the timing of histone gene activation during the cell cycle. Furthermore, our data indicate that HiNF-P/H4TF-2 may functionally compensate for HiNF-M/IRF-2 at Site II to regulate histone H4 gene transcription in HeLa S3 cervical carcinoma cells during early S phase. We postulate that HiNF-D (CDP-cut/cyclin A/CDC2/pRB containing complex) promotes HiNF-M/IRF-2 (and/or HiNF-P/H4TF-2) dependent histone H4 gene activation at the G1/S phase transition and attenuates H4 gene transcription at later cell cycle stages. The mechanistic division in the gene regulatory functions of the three H4-Site II binding proteins may ensure that histone H4 gene expression is stringently coupled with the onset of S phase in response to growth factor/cytokine-induced cell cycle progression.
    Source

    J Cell Physiol. 1998 Dec;177(3):453-64.

    DOI
    10.1002/(SICI)1097-4652(199812)177:3<453::AID-JCP8>3.0.CO;2-F
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33987
    PubMed ID
    9808153
    Related Resources

    Link to article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1002/(SICI)1097-4652(199812)177:3<453::AID-JCP8>3.0.CO;2-F
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