TY - JOUR
T1 - Mte1 interacts with Mph1 and promotes crossover recombination and telomere maintenance
AU - Pinela da Silva, Sonia Cristina
AU - Altmannova, Veronika
AU - Luke-Glaser, Sarah
AU - Henriksen, Peter
AU - Gallina, Irene
AU - Yang, Xuejiao
AU - Choudhary, Chuna Ram
AU - Luke, Brian
AU - Krejci, Lumir
AU - Lisby, Michael
N1 - © 2016 Silva et al.; Published by Cold Spring Harbor Laboratory Press.
PY - 2016/3/15
Y1 - 2016/3/15
N2 - 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.
AB - 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.
U2 - 10.1101/gad.276204.115
DO - 10.1101/gad.276204.115
M3 - Journal article
C2 - 26966248
SN - 0890-9369
VL - 30
SP - 700
EP - 717
JO - Genes & Development
JF - Genes & Development
IS - 6
ER -