http://www.cnr.it/ontology/cnr/individuo/prodotto/ID11606
Unprotected Drosophila melanogaster telomeres activate the spindle assembly checkpoint. (Articolo in rivista)
- Type
- Label
- Unprotected Drosophila melanogaster telomeres activate the spindle assembly checkpoint. (Articolo in rivista) (literal)
- Anno
- 2008-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1038/ing.2007.64 (literal)
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- Musarò M; Ciapponi L; Fasulo B; Gatti M; Cenci G. (literal)
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Musarò M; Ciapponi L; Gatti M;.: Istituto di Biologia e Patologia Molecolari del CNR and Dipartimento di Genetica e Biologia Molecolare, Universita` di Roma 'La Sapienza
Fasulo B.:Molecular Cell and Developmental Biology, University of California, Santa Cruz, California 95064, USA
Cenci G.: Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali (DiSTeBA), Universita` del Salento, Lecce 73100 (literal)
- Titolo
- Unprotected Drosophila melanogaster telomeres activate the spindle assembly checkpoint. (literal)
- Abstract
- In both yeast and mammals, uncapped telomeres activate the DNA damage response (DDR) and undergo end-to-end fusion. Previous work has shown that the Drosophila HOAP protein, encoded by the caravaggio (cav) gene, is required to prevent telomeric fusions. Here we show that HOAP-depleted telomeres activate both the DDR and the spindle assembly checkpoint (SAC). The cell cycle arrest elicited by the DDR was alleviated by mutations in mei-41 (ATR), mus304 (ATRIP), grp (Chk1) and rad50 but not by mutations in tefu (ATM). The SAC was partially overridden by mutations in zw10 and bubR1 but also by mutations in mei-41, mus304, rad50, grp and tefu. As expected from SAC activation, the SAC proteins Zw10, Zwilch, BubR1 and Cenp-meta (Cenp-E) accumulated at the kinetochores of cav mutant cells. Surprisingly, BubR1 also accumulated at cav mutant telomeres in a mei-41, mus304, rad50, grp and tefu-dependent manner. Our results collectively suggest that recruitment of BubR1 by dysfunctional telomeres inhibits Cdc20/APC function, preventing the metaphase-to-anaphase transition. (literal)
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