The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.

The Fanconi anemia (FA) core complex promotes the tolerance/repair of DNA damage at stalled replication forks by catalyzing the monoubiquitination of FANCD2 and FANCI. Intriguingly, the core complex component FANCM also catalyzes branch migration of model Holliday junctions and replication forks in...

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Main Authors: Sun, W, Nandi, S, Osman, F, Ahn, J, Jakovleska, J, Lorenz, A, Whitby, M
Format: Journal article
Language:English
Published: 2008
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author Sun, W
Nandi, S
Osman, F
Ahn, J
Jakovleska, J
Lorenz, A
Whitby, M
author_facet Sun, W
Nandi, S
Osman, F
Ahn, J
Jakovleska, J
Lorenz, A
Whitby, M
author_sort Sun, W
collection OXFORD
description The Fanconi anemia (FA) core complex promotes the tolerance/repair of DNA damage at stalled replication forks by catalyzing the monoubiquitination of FANCD2 and FANCI. Intriguingly, the core complex component FANCM also catalyzes branch migration of model Holliday junctions and replication forks in vitro. Here we have characterized the ortholog of FANCM in fission yeast Fml1 in order to understand the physiological significance of this activity. We show that Fml1 has at least two roles in homologous recombination-it promotes Rad51-dependent gene conversion at stalled/blocked replication forks and limits crossing over during mitotic double-strand break repair. In vitro Fml1 catalyzes both replication fork reversal and D loop disruption, indicating possible mechanisms by which it can fulfill its pro- and antirecombinogenic roles.
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spelling oxford-uuid:88643850-a872-4265-8b5d-59a556615b392022-03-26T22:16:58ZThe FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:88643850-a872-4265-8b5d-59a556615b39EnglishSymplectic Elements at Oxford2008Sun, WNandi, SOsman, FAhn, JJakovleska, JLorenz, AWhitby, MThe Fanconi anemia (FA) core complex promotes the tolerance/repair of DNA damage at stalled replication forks by catalyzing the monoubiquitination of FANCD2 and FANCI. Intriguingly, the core complex component FANCM also catalyzes branch migration of model Holliday junctions and replication forks in vitro. Here we have characterized the ortholog of FANCM in fission yeast Fml1 in order to understand the physiological significance of this activity. We show that Fml1 has at least two roles in homologous recombination-it promotes Rad51-dependent gene conversion at stalled/blocked replication forks and limits crossing over during mitotic double-strand break repair. In vitro Fml1 catalyzes both replication fork reversal and D loop disruption, indicating possible mechanisms by which it can fulfill its pro- and antirecombinogenic roles.
spellingShingle Sun, W
Nandi, S
Osman, F
Ahn, J
Jakovleska, J
Lorenz, A
Whitby, M
The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.
title The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.
title_full The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.
title_fullStr The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.
title_full_unstemmed The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.
title_short The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.
title_sort fancm ortholog fml1 promotes recombination at stalled replication forks and limits crossing over during dna double strand break repair
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