ARF triggers senescence in Brca2-deficient cells by altering the spectrum of p53 transcriptional targets View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-10-28

AUTHORS

Ana Rita Carlos, Jose Miguel Escandell, Panagiotis Kotsantis, Natsuko Suwaki, Peter Bouwman, Sophie Badie, Cecilia Folio, Javier Benitez, Gonzalo Gomez-Lopez, David G. Pisano, Jos Jonkers, Madalena Tarsounas

ABSTRACT

ARF is a tumour suppressor activated by oncogenic stress, which stabilizes p53. Although p53 is a key component of the response to DNA damage, a similar function for ARF has not been ascribed. Here we show that primary mouse and human cells lacking the tumour suppressor BRCA2 accumulate DNA damage, which triggers checkpoint signalling and ARF activation. Furthermore, senescence induced by Brca2 deletion in primary mouse and human cells is reversed by the loss of ARF, a phenotype recapitulated in cells lacking RAD51. Surprisingly, ARF is not necessary for p53 accumulation per se but for altering the spectrum of genes activated by this transcription factor. Specifically, ARF enables p53 transcription of Dusp4 and Dusp7, which encode a pair of phosphatases known to inactivate the MAP kinases ERK1/2. Our results ascribe a previously unanticipated function to the ARF tumour suppressor in genome integrity, controlled by replicative stress and ATM/ATR-dependent checkpoint responses. More... »

PAGES

2697

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    4

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms3697

    DOI

    http://dx.doi.org/10.1038/ncomms3697

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1047103985

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/24162189


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