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  • American Association for the Advancement of Science (AAAS)  (2)
  • 1990-1994  (2)
  • 1
    Publication Date: 1990-11-09
    Description: The regulation of DNA replication during the eukaryotic cell cycle was studied in a system where cell free replication of simian virus 40 (SV40) DNA was used as a model for chromosome replication. A factor, RF-S, was partially purified from human S phase cells based on its ability to activate DNA replication in extracts from G1 cells. RF-S contained a human homologue of the Schizosaccharomyces pombe p34cdc2 kinase, and this kinase was necessary for RF-S activity. The limiting step in activation of the p34 kinase at the G1 to S transition may be its association with a cyclin since addition of cyclin A to a G1 extract was sufficient to start DNA replication. These observations suggest that the role of p34cdc2 in controlling the start of DNA synthesis has been conserved in evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉D'Urso, G -- Marraccino, R L -- Marshak, D R -- Roberts, J M -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):786-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Sciences, Fred Hutchinson Cancer Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173140" target="_blank"〉PubMed〈/a〉
    Keywords: Burkitt Lymphoma ; CDC2 Protein Kinase/genetics/*physiology ; *Cell Cycle ; Cyclins/pharmacology ; *DNA Replication ; Humans ; Interphase ; Phosphorylation ; Schizosaccharomyces/enzymology ; Simian virus 40/*genetics/physiology ; Tumor Cells, Cultured ; *Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1991-02-08
    Description: To understand the principles of control and selectivity in gene expression, the biochemical mechanisms by which promoter- and enhancer-binding factors regulate transcription by RNA polymerase II were analyzed. A general observed repressor of transcription was purified and identified as histone H1. Since many aspects of H1 binding to naked DNA resemble its interaction with chromatin, purified H1 bound to naked DNA was used as a model for the repressed state of the DNA template. Three sequence-specific transcription factors, Sp1, GAL4-VP16, and GAGA factor, were shown to counteract H1-mediated repression (antirepression). In addition, Sp1 and GAL4-VP16, but not the GAGA factor, activated transcription in the absence of H1. Therefore, true activation and antirepression appear to be distinct activities of sequence-specific factors. Furthermore, transcription antirepression by GAL4-VP16 was sustained for several rounds of transcription. These findings, together with previous studies on H1, suggest that H1 participates in repression of the genome in the ground state and that sequence-specific transcription factors induce selected genes by a combination of true activation and release of basal repression that is mediated at least in part by H1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Croston, G E -- Kerrigan, L A -- Lira, L M -- Marshak, D R -- Kadonaga, J T -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):643-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1899487" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cattle ; Cell-Free System ; DNA-Binding Proteins/physiology ; Drosophila melanogaster/genetics ; *Gene Expression Regulation ; HeLa Cells ; Histones/genetics/*physiology ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Nucleosomes/physiology ; RNA Polymerase II/*physiology ; Regulatory Sequences, Nucleic Acid ; Repressor Proteins/physiology ; Templates, Genetic ; Transcription Factors/*physiology ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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