| Texto completo | |
| Autor(es): Mostrar menos - |
Lerner, Leticia K.
;
Francisco, Guilherme
;
Soltys, Daniela T.
;
Rocha, Clarissa R. R.
;
Quinet, Annabel
;
Vessoni, Alexandre T.
;
Castro, Ligia P.
;
David, Taynah I. P.
;
Bustos, Silvina O.
;
Strauss, Bryan E.
;
Gottifredi, Vanesa
;
Stary, Anne
;
Sarasin, Alain
;
Chammas, Roger
;
Menck, Carlos F. M.
Número total de Autores: 15
|
| Tipo de documento: | Artigo Científico |
| Fonte: | Nucleic Acids Research; v. 45, n. 3, p. 1270-1280, FEB 2017. |
| Citações Web of Science: | 11 |
| Resumo | |
Genome lesions trigger biological responses that help cells manage damaged DNA, improving cell survival. Pol eta is a translesion synthesis (TLS) polymerase that bypasses lesions that block replicative polymerases, avoiding continued stalling of replication forks, which could lead to cell death. p53 also plays an important role in preventing cell death after ultraviolet (UV) light exposure. Intriguingly, we show that p53 does so by favoring translesion DNA synthesis by pol eta. In fact, the p53-dependent induction of pol eta in normal and DNA repair-deficient XP-C human cells afterUV exposure has a protective effect on cell survival after challenging UV exposures, which was absent in p53-and Pol H-silenced cells. Viability increase was associated with improved elongation of nascent DNA, indicating the protective effect was due to more efficient lesion bypass by pol eta. This protection was observed in cells proficient or deficient in nucleotide excision repair, suggesting that, from a cell survival perspective, proper bypass of DNA damage can be as relevant as removal. These results indicate p53 controls the induction of pol eta in DNA damaged human cells, resulting in improved TLS and enhancing cell tolerance to DNA damage, which parallels SOS responses in bacteria. (AU) | |
| Processo FAPESP: | 14/15982-6 - Consequências de deficiências de reparo de lesões no genoma |
| Beneficiário: | Carlos Frederico Martins Menck |
| Linha de fomento: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 13/21075-9 - Participação da NADPH oxidase 2 induzida pelo estrogênio em lesões no DNA e na regulação da autofagia em linhagem celular de mama |
| Beneficiário: | Carlos Frederico Martins Menck |
| Linha de fomento: | Auxílio à Pesquisa - Pesquisador Visitante - Brasil |