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J Biol Chem ; 283(15): 9844-51, 2008 Apr 11.
Artículo en Inglés | MEDLINE | ID: mdl-18263878

RESUMEN

The disease Fanconi anemia is a genome instability syndrome characterized by cellular sensitivity to DNA interstrand cross-linking agents, manifest by decreased cellular survival and chromosomal aberrations after such treatment. There are at least 13 proteins acting in the pathway, with the FANCD2 protein apparently functioning as a late term effecter in the maintenance of genome stability. We find that the chromatin remodeling protein, Tip60, interacts directly with the FANCD2 protein in a yeast two-hybrid system. This interaction has been confirmed by co-immunoprecipitation and co-localization using both endogenous and epitope-tagged FANCD2 and Tip60 from human cells. The observation of decreased cellular survival after exposure to mitomycin C in normal fibroblasts depleted for Tip60 indicates a direct function in interstrand cross-link repair. The coincident function of Tip60 and FANCD2 in one pathway is supported by the finding that depletion of Tip60 in Fanconi anemia cells does not increase sensitivity to DNA cross-links. However, depletion of Tip60 did not reduce monoubiquitination of FANCD2 or its localization to nuclear foci following DNA damage. The observations indicate that Fanconi anemia proteins act in concert with chromatin remodeling functions to maintain genome stability after DNA cross-link damage.


Asunto(s)
Núcleo Celular/metabolismo , Ensamble y Desensamble de Cromatina/fisiología , Reparación del ADN/fisiología , Proteína del Grupo de Complementación D2 de la Anemia de Fanconi/metabolismo , Histona Acetiltransferasas/metabolismo , Transporte Activo de Núcleo Celular/efectos de los fármacos , Transporte Activo de Núcleo Celular/genética , Línea Celular , Núcleo Celular/genética , Supervivencia Celular/efectos de los fármacos , Supervivencia Celular/genética , Reactivos de Enlaces Cruzados/farmacología , Daño del ADN/efectos de los fármacos , Daño del ADN/genética , Reparación del ADN/efectos de los fármacos , Anemia de Fanconi/genética , Anemia de Fanconi/metabolismo , Proteína del Grupo de Complementación D2 de la Anemia de Fanconi/genética , Inestabilidad Genómica/efectos de los fármacos , Inestabilidad Genómica/genética , Histona Acetiltransferasas/genética , Humanos , Lisina Acetiltransferasa 5 , Mitomicina/farmacología , Ubiquitinación/efectos de los fármacos , Ubiquitinación/fisiología
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