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    Multiple pathways differentially regulate global oxidative stress responses in fission yeast.

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    Authors
    Chen, Dongrong
    Wilkinson, Caroline R M
    Watt, Stephen
    Penkett, Christopher J
    Toone, W Mark
    Jones, Nic
    Bähler, Jürg
    Affiliation
    Cancer Research UK Fission Yeast Functional Genomics Group, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, United Kingdom.
    Issue Date
    2008-01
    
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    Abstract
    Cellular protection against oxidative damage is relevant to ageing and numerous diseases. We analyzed the diversity of genome-wide gene expression programs and their regulation in response to various types and doses of oxidants in Schizosaccharomyces pombe. A small core gene set, regulated by the AP-1-like factor Pap1p and the two-component regulator Prr1p, was universally induced irrespective of oxidant and dose. Strong oxidative stresses led to a much larger transcriptional response. The mitogen-activated protein kinase (MAPK) Sty1p and the bZIP factor Atf1p were critical for the response to hydrogen peroxide. A newly identified zinc-finger protein, Hsr1p, is uniquely regulated by all three major regulatory systems (Sty1p-Atf1p, Pap1p, and Prr1p) and in turn globally supports gene expression in response to hydrogen peroxide. Although the overall transcriptional responses to hydrogen peroxide and t-butylhydroperoxide were similar, to our surprise, Sty1p and Atf1p were less critical for the response to the latter. Instead, another MAPK, Pmk1p, was involved in surviving this stress, although Pmk1p played only a minor role in regulating the transcriptional response. These data reveal a considerable plasticity and differential control of regulatory pathways in distinct oxidative stress conditions, providing both specificity and backup for protection from oxidative damage.
    Citation
    Multiple pathways differentially regulate global oxidative stress responses in fission yeast. 2008, 19 (1):308-17 Mol. Biol. Cell
    Journal
    Molecular Biology of the Cell
    URI
    http://hdl.handle.net/10541/56017
    DOI
    10.1091/mbc.E07-08-0735
    PubMed ID
    18003976
    Type
    Article
    Language
    en
    ISSN
    1939-4586
    ae974a485f413a2113503eed53cd6c53
    10.1091/mbc.E07-08-0735
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research
    Cell Regulation

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