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    Cell Cycle. 2007 Jul 1;6(13):1655-62. Epub 2007 May 8.

    Bin1 homolog hob1 supports a Rad6-Set1 pathway of transcriptional repression in fission yeast.

    Ramalingam A, Prendergast GC.

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    Lankenau Institute for Medical Research, Wynnewood, Pennsylvania 19096, USA.

    Abstract

    Bin1 encodes a mammalian BAR adapter protein with a nuclear anti-oncogenic function that is poorly understood. To gain functional insights, we investigated the role of the fission yeast homolog hob1+ in growth arrest and survival of cells treated with phleomycin, a DNA damaging drug. Unlike wild-type cells, hob1delta cells treated with phleomycin displayed a defective growth arrest phenotype, elongating abnormally without septation or cytokinesis and eventually losing viability. Genetic investigations suggested that the survival defect in hob1delta cells reflected a deficiency in a Rad6 pathway involving histone methyltransferase Set1 that leads to transcriptional repression. In support of this connection, transcription of telomeric and centromeric heterochromatin that is normally silenced by a Rad6/Set1-dependent mechanism was aberrantly activated in hob1delta cells. Taken together, these findings suggest that hob1+ may support a mechanism of transcriptional repression possibly relevant to the role of Bin1 in cancer suppression.

    PMID:
    17611416
    [PubMed - indexed for MEDLINE]
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