Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos (Articolo in rivista)

Type
Label
  • Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos (Articolo in rivista) (literal)
Anno
  • 2006-01-01T00:00:00+01:00 (literal)
Alternative label
  • Holway AH; Kim SH; La Volpe A; Michael WM. (2006)
    Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos
    in The journal of cell biology (Online)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Holway AH; Kim SH; La Volpe A; Michael WM. (literal)
Pagina inizio
  • 999 (literal)
Pagina fine
  • 1008 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 172 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • The Biological Laboratories, Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138 Istituto di Genetica e Biofisica \"Adriano Buzzati-Traverso,\" Consiglio Nazionale delle Ricerche, 80125 Naples, Italy (literal)
Titolo
  • Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos (literal)
Abstract
  • In most cells, the DNA damage checkpoint delays cell division when replication is stalled by DNA damage. In early Caenorhabditis elegans embryos, however, the checkpoint responds to developmental signals that control the timing of cell division, and checkpoint activation by nondevelopmental inputs disrupts cell cycle timing and causes embryonic lethality. Given this sensitivity to inappropriate checkpoint activation, we were interested in how embryos respond to DNA damage. We demonstrate that the checkpoint response to DNA damage is actively silenced in embryos but not in the germ line. Silencing requires rad-2, gei-17, and the polh-1 translesion DNA polymerase, which suppress replication fork stalling and thereby eliminate the checkpoint-activating signal. These results explain how checkpoint activation is restricted to developmental signals during embryogenesis and insulated from DNA damage. They also show that checkpoint activation is not an obligatory response to DNA damage and that pathways exist to bypass the checkpoint when survival depends on uninterrupted progression through the cell cycle. (literal)
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