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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,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1987 to 6 months ago
Freely Accessible Science Journals
from 1987-03-01 to 6 months ago
PubMed Central
from 1997 to 6 months ago
Europe PubMed Central
from 1997 to 6 months ago
Open Access Digital Library
from 1987-03-01
Open Access Digital Library
from 1987-01-01
- MeSH
- Crossing Over, Genetic genetics MeSH
- DEAD-box RNA Helicases genetics metabolism MeSH
- Gene Deletion MeSH
- Stress, Physiological genetics MeSH
- Telomere Homeostasis genetics MeSH
- Telomere-Binding Proteins genetics metabolism MeSH
- Saccharomyces cerevisiae Proteins genetics metabolism MeSH
- Saccharomyces cerevisiae genetics metabolism MeSH
- Protein Transport MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
Department of Biology Masaryk University CZ 62500 Brno Czech Republic
Department of Biology University of Copenhagen DK 2200 Copenhagen N Denmark
Institute of Molecular Biology gGmbH 55128 Mainz Germany
National Centre for Biomolecular Research Masaryk University CZ 62500 Brno Czech Republic
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- $a 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.
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