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Your search keyword '"Osman, Fekret"' showing total 3 results
Start Over Author "Osman, Fekret" Journal molecular cell
3 results on '"Osman, Fekret"'

1. A histone-fold complex and FANCM form a conserved DNA-remodeling complex to maintain genome stability.

Author

Yan Z, Delannoy M, Ling C, Daee D, Osman F, Muniandy PA, Shen X, Oostra AB, Du H, Steltenpool J, Lin T, Schuster B, Décaillet C, Stasiak A, Stasiak AZ, Stone S, Hoatlin ME, Schindler D, Woodcock CL, Joenje H, Sen R, de Winter JP, Li L, Seidman MM, Whitby MC, Myung K, Constantinou A, and Wang W more...

Subjects
Amino Acid Sequence, Animals, Cell Line, Chickens, DNA genetics, DNA Damage, DNA Helicases chemistry, DNA Helicases genetics, DNA Replication, DNA-Binding Proteins genetics, DNA-Binding Proteins metabolism, Evolution, Molecular, Fanconi Anemia Complementation Group Proteins, Humans, Molecular Sequence Data, Protein Binding, Saccharomyces cerevisiae genetics, Saccharomyces cerevisiae metabolism, Schizosaccharomyces genetics, Schizosaccharomyces metabolism, Sequence Alignment, Sister Chromatid Exchange, DNA metabolism, DNA Helicases metabolism, Genomic Instability, Histones metabolism, Protein Folding, Protein Multimerization
Abstract

FANCM remodels branched DNA structures and plays essential roles in the cellular response to DNA replication stress. Here, we show that FANCM forms a conserved DNA-remodeling complex with a histone-fold heterodimer, MHF. We find that MHF stimulates DNA binding and replication fork remodeling by FANCM. In the cell, FANCM and MHF are rapidly recruited to forks stalled by DNA interstrand crosslinks, and both are required for cellular resistance to such lesions. In vertebrates, FANCM-MHF associates with the Fanconi anemia (FA) core complex, promotes FANCD2 monoubiquitination in response to DNA damage, and suppresses sister-chromatid exchanges. Yeast orthologs of these proteins function together to resist MMS-induced DNA damage and promote gene conversion at blocked replication forks. Thus, FANCM-MHF is an essential DNA-remodeling complex that protects replication forks from yeast to human., ((c) 2010 Elsevier Inc. All rights reserved.) more...

Published
2010
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2. The FANCM ortholog Fml1 promotes recombination at stalled replication forks and limits crossing over during DNA double-strand break repair.

Author

Sun W, Nandi S, Osman F, Ahn JS, Jakovleska J, Lorenz A, and Whitby MC

Subjects
Crossing Over, Genetic, DNA Helicases genetics, DNA Replication, DNA, Cruciform, DNA, Fungal chemistry, DNA, Fungal genetics, DNA, Fungal metabolism, Fanconi Anemia genetics, Fanconi Anemia metabolism, Gene Conversion, Genes, Fungal, Humans, Mutation, Recombination, Genetic, Schizosaccharomyces pombe Proteins genetics, DNA Breaks, Double-Stranded, DNA Helicases metabolism, DNA Repair, Schizosaccharomyces genetics, Schizosaccharomyces metabolism, Schizosaccharomyces pombe Proteins metabolism
Abstract

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. more...

Published
2008
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3. Generating crossovers by resolution of nicked Holliday junctions: a role for Mus81-Eme1 in meiosis.

Author

Osman F, Dixon J, Doe CL, and Whitby MC

Subjects
Crossing Over, Genetic genetics, DNA genetics, DNA-Binding Proteins genetics, Endonucleases genetics, Nucleic Acid Conformation, Saccharomyces cerevisiae Proteins, Schizosaccharomyces genetics, Schizosaccharomyces pombe Proteins genetics, DNA metabolism, DNA-Binding Proteins metabolism, Endonucleases metabolism, Meiosis genetics, Recombination, Genetic genetics, Schizosaccharomyces enzymology, Schizosaccharomyces pombe Proteins metabolism
Abstract

The double Holliday junction (dHJ) is generally regarded to be a key intermediate of meiotic recombination, whose resolution is critical for the formation of crossover recombinants. In fission yeast, the Mus81-Eme1 endonuclease has been implicated in resolving dHJs. Consistent with this role, we show that Mus81-Eme1 is required for generating meiotic crossovers. However, purified Mus81-Eme1 prefers to cleave junctions that mimic those formed during the transition from double-strand break to dHJ. Crucially, these junctions are cleaved by Mus81-Eme1 in precisely the right orientation to guarantee the formation of a crossover every time. These data demonstrate how crossovers could arise without forming or resolving dHJs using an enzyme that is widely conserved amongst eukaryotes. more...

Published
2003
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