Mte1 interacts with Mph1 and promotes crossover recombination and telomere maintenance

Mph1 is a member of the conserved FANCM family of DNA motor proteins that play key roles in genome maintenance processes underlying Fanconi anemia, a cancer predisposition syndrome in humans. Here, we identify Mte1 as a novel interactor of the Mph1 helicase in Saccharomyces cerevisiae. In vitro, Mte...

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Detalhes bibliográficos
Autores: Silva, Sonia, Altmannova, Veronika, Luke Glaser, Sarah, Henriksen, Peter, Gallina, Irene, Yang, Xuejiao, Choudhary, Chunaram, Luke, Brian, Krejci, Lumir, Lisby, Michael
Tipo de documento: artigo
Estado:Versión aceptada para publicación
Data de publicação:2016
País:España
Recursos:Universidad de Sevilla (US)
Repositório:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/81686
Acesso em linha:https://hdl.handle.net/11441/81686
https://doi.org/10.1101/gad.276204.115
Access Level:Acceso aberto
Palavra-chave:Homologous recombination
Telomere maintenance
Genome integrity
DNA repair
Mph1
Mte1
Descrição
Resumo:Mph1 is a member of the conserved FANCM family of DNA motor proteins that play key roles in genome maintenance processes underlying Fanconi anemia, a cancer predisposition syndrome in humans. Here, we identify Mte1 as a novel interactor of the Mph1 helicase in Saccharomyces cerevisiae. In vitro, Mte1 (Mph1-associated telomere maintenance protein 1) binds directly to DNA with a preference for branched molecules such as D loops and fork structures. In addition, Mte1 stimulates the helicase and fork regression activities of Mph1 while inhibiting the ability of Mph1 to dissociate recombination intermediates. Deletion of MTE1 reduces crossover recombination and suppresses the sensitivity of mph1Δ mutant cells to replication stress. Mph1 and Mte1 interdependently colocalize atDNAdamage-induced foci and dysfunctional telomeres, and MTE1 deletion results in elongated telomeres. Taken together, our data indicate that Mte1 plays a role in regulation of crossover recombination, response to replication stress, and telomere maintenance.