Nucleosome-driven transcription factor binding and gene regulation

In fission yeast cells, Cds1 is the effector kinase of the DNA replication checkpoint. We previously showed that when the DNA replication checkpoint is activated, the repressor Yox1 is phosphorylated and inactivated by Cds1, resulting in activation of MluI-binding factor (MBF)-dependent transcriptio...

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Detalhes bibliográficos
Autores: Ballaré, Cecilia Julia, Castellano, Giancarlo, Gaveglia, Laura, Althammer, Sonja Daniela, González-Vallinas Rostes, Juan, 1983-, Eyras Jiménez, Eduardo, Le Dily, François, Zaurín Quer, Roser, Soronellas, Daniel, Vicent, Guillermo Pablo, Beato, Miguel
Tipo de documento: artigo
Estado:Versão publicada
Data de publicação:2013
País:España
Recursos:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositório:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:10230/25285
Acesso em linha:http://hdl.handle.net/10230/25285
http://dx.doi.org/10.1016/j.molcel.2012.10.019
Access Level:Acceso aberto
Palavra-chave:Gens humans Mapatge
Cromatina
Descrição
Resumo:In fission yeast cells, Cds1 is the effector kinase of the DNA replication checkpoint. We previously showed that when the DNA replication checkpoint is activated, the repressor Yox1 is phosphorylated and inactivated by Cds1, resulting in activation of MluI-binding factor (MBF)-dependent transcription. This is essential to reinitiate DNA synthesis and for correct G1-to-S transition. Here we show that Cdc10, which is an essential part of the MBF core, is the target of the DNA damage checkpoint. When fission yeast cells are treated with DNA-damaging agents, Chk1 is activated and phosphorylates Cdc10 at its carboxy-terminal domain. This modification is responsible for the repression of MBF-dependent transcription through induced release of MBF from chromatin. This inactivation of MBF is important for survival of cells challenged with DNA-damaging agents. Thus Yox1 and Cdc10 couple normal cell cycle regulation in unperturbed conditions and the DNA replication and DNA damage checkpoints into a single transcriptional complex.