4.7 Article

Mte1 interacts with Mph1 and promotes crossover recombination and telomere maintenance

Journal

GENES & DEVELOPMENT
Volume 30, Issue 6, Pages 700-717

Publisher

COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.276204.115

Keywords

homologous recombination; telomere maintenance; genome integrity; DNA repair; Mph1; Mte1

Funding

  1. Danish Agency for Science, Technology, and Innovation
  2. Villum Foundation
  3. Lundbeck Foundation
  4. European Research Council (ERC)
  5. Danish National Research Foundation [DNRF115]
  6. Chinese Scholarship Council
  7. Fundacao para a Ciencia e Tecnologia (FCT)
  8. European Regional Development Fund [CZ.1.05/1.1.00/02.0123]
  9. Faculty of Medicine Masaryk University
  10. EMBO Young Investigator program
  11. Novo Nordisk Foundation [NNF14CC0001]
  12. [GACR13-26629S]
  13. [GACR207/12/2323]
  14. Novo Nordisk Foundation Center for Protein Research [PI Chunaram Choudhary] Funding Source: researchfish
  15. Villum Fonden [00011407] Funding Source: researchfish

Ask authors/readers for more resources

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 mph1 Delta mutant cells to replication stress. Mph1 and Mte1 interdependently colocalize at DNA damage-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.

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