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Mte1 interacts with Mph1 and promotes crossover recombination and telomere maintenance

S. Silva, V. Altmannova, S. Luke-Glaser, P. Henriksen, I. Gallina, X. Yang, C. Choudhary, B. Luke, L. Krejci, M. Lisby,

. 2016 ; 30 (6) : 700-17. [pub] 20160310

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc16027596
E-zdroje Online Plný text

NLK Free Medical Journals od 1987 do Před 6 měsíci
Freely Accessible Science Journals od 1987-03-01 do Před 6 měsíci
PubMed Central od 1997 do Před 6 měsíci
Europe PubMed Central od 1997 do Před 6 měsíci
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Open Access Digital Library od 1987-01-01

Odkazy

PubMed 26966248
DOI 10.1101/gad.276204.115
Knihovny.cz E-zdroje

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 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.

Citace poskytuje Crossref.org

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