The cell response to replicationdefects affects alternative splicing programs and cell morphology (Abstract/Poster in atti di convegno)

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  • The cell response to replicationdefects affects alternative splicing programs and cell morphology (Abstract/Poster in atti di convegno) (literal)
Anno
  • 2013-01-01T00:00:00+01:00 (literal)
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  • Oliverio M, Cabrini M, Leva V, Biamonti G, Montecucco A (2013)
    The cell response to replicationdefects affects alternative splicing programs and cell morphology
    in Celebrating the 50th anniversary of the Replication Theory, Institut Pasteur, Parigi, F, 25-28 marzo 2013
    (literal)
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  • Oliverio M, Cabrini M, Leva V, Biamonti G, Montecucco A (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#titoloVolume
  • Abstract Book (literal)
Note
  • Poster (literal)
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  • IGM CNR (literal)
Titolo
  • The cell response to replicationdefects affects alternative splicing programs and cell morphology (literal)
Abstract
  • Cells established from a patient with hypomorphic mutations of DNA ligase I gene show a delay in the maturation of replicative intermediates resulting in the accumulation of single and double-stranded breaks. In these cells the ataxia telangiectasia mutated protein kinase (ATM) and its downstream kinase Chk2 are constitutively phosphorylated at a basal level (1). Using DNA ligase I-defective 46BR.1G1 cells as system model to study the cell response to replication-mediated DNA damage, we have recently demonstrated that the damage elicited by DNA ligase I deficiency causes a change in the phosphorylation pattern of the alternative splicing factor SRSF1 (SF2/ASF). As a consequence, SRSF1 target transcripts, such as the tumorigenic Recepteur d'Origine Nantais (RON) and Caspase 9, undergo a change in their alternative splicing program allowing the survival of damaged cells (2). The basal level of ATM activation is also required to promote a change of cell morphology unveiling a link between replication defects and the structural organization of the cell. 1. Soza S., Leva V. et al. Mol Cell Biol (2009) 29:2032-41 2. Leva V., Giuliano S. et al Nucleic Acids Res (2012) 40:1106-17 (literal)
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