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    Suppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control.

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    Authors
    Tallada, Victor A
    Bridge, Alan J
    Emery, Patrick A
    Hagan, Iain M
    Affiliation
    CRUK Cell Division Group, Paterson Institute for Cancer Research, University of Manchester, Manchester M20 4BX, United Kingdom.
    Issue Date
    2007-05
    
    Metadata
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    Abstract
    Cdc25 phosphatase primes entry to mitosis by removing the inhibitory phosphate that is transferred to mitosis promoting factor (MPF) by Wee1 related kinases. A positive feedback loop then boosts Cdc25 and represses Wee1 activities to drive full-scale MPF activation and commitment to mitosis. Dominant mutations in the Schizosaccharomyces pombe spindle pole body (SPB) component Cut12 enable cdc25.22 mutants to overcome a G2 arrest at 36 degrees and enter mitosis. The recessive temperature-sensitive cut12.1 mutation results in the formation of monopolar spindles in which the spindle pole marker Sad1 is enriched on the nonfunctional SPB at 36 degrees . We identified mutations at five loci that suppressed the lethality of the recessive cut12.1 mutation at 36 degrees and conferred lethality at 20 degrees . Three of the five mutations led to the formation of monopolar spindles at restrictive temperatures, affected cell size at commitment to mitosis, and generated multiple Sad1 foci at nuclear periphery. The five loci, tfb2.rt1, tfb5.rt5, pla1.rt3, rpl4301.rt4, and rot2.1, and multicopy suppressors, including tfb1(+) and dbp10(+), are involved in transcription, translation, or RNA processing, prompting us to establish that elevating Cdc25 levels with the dominant cdc25.d1 allele, suppressed cut12.1. Thus, rot mutants provide a further link between protein production and cell-cycle progression.
    Citation
    Suppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control. 2007, 176 (1):73-83 Genetics
    Journal
    Genetics
    URI
    http://hdl.handle.net/10541/71916
    DOI
    10.1534/genetics.107.072090
    PubMed ID
    17409062
    Type
    Article
    Language
    en
    ISSN
    0016-6731
    ae974a485f413a2113503eed53cd6c53
    10.1534/genetics.107.072090
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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