Budding yeast Mph1 promotes sister chromatid interactions by a mechanism involving strand invasion

Ede, Christopher; Rudolph, Christian J.; Lehmann, Sabrina; Schürer, K. Anke; Kramer, Wilfried

doi:10.1016/j.dnarep.2010.09.009

Cited by 10 publications

(13 citation statements)

References 83 publications

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“…The complex func tions early in homologous recombination, probably stabilizing the D loops [16,17]. The product of the MPH1 gene possesses helicase activity and functions during the formation and degradation of D loops aris ing during repair of blocked replication forks [18]. The Mhp1 protein and the Shu1 and Mms2 complexes may act independently to organize recombination intermediates [19].…”

Section: Introductionmentioning

confidence: 99%

Interactions of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae

et al. 2012

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Section: Introductionmentioning

confidence: 99%

Interactions of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae

et al. 2012

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“…Nevertheless, Mph1 may also affect replication by additional means. Recent genetic evidence suggests that Mph1 functions with the DNA motor protein Rad54 in extending the Rad51-made D loop to promote sister chromatid association (Ede et al 2011). The sensitivity of fml1 and mph1 mutants to replication-blocking agents likely stems from the simultaneous ablation of multiple mechanisms of fork preservation and recombinational repair (Scheller et al 2000;Sun et al 2008).…”

Section: Roles Of Schizosaccharomyces Pombe Fml1 and Saccharomyces Cementioning

confidence: 99%

Functions and regulation of the multitasking FANCM family of DNA motor proteins

2015

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Members of the conserved FANCM family of DNA motor proteins play key roles in genome maintenance processes. FANCM supports genome duplication and repair under different circumstances and also functions in the ATR-mediated DNA damage checkpoint. Some of these roles are shared among lower eukaryotic family members. Human FANCM has been linked to Fanconi anemia, a syndrome characterized by cancer predisposition, developmental disorder, and bone marrow failure. Recent studies on human FANCM and its orthologs from other organisms have provided insights into their biological functions, regulation, and collaboration with other genome maintenance factors. This review summarizes the progress made, with the goal of providing an integrated view of the functions and regulation of these enzymes in humans and model organisms and how they advance our understanding of genome maintenance processes.

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“…Sc-MPH1 is epistatic to a number of budding yeast homologous recombination (HR) genes, and the somatic HR rate is increased in mph1 mutant cells (Schürer et al, 2004). Recently, it was shown that Mph1 participates in D-loop formation in HR, together with the recombinase Rad54 (for radiation sensitive54) (Panico et al, 2010;Ede et al, 2011). In double mutants of MPH1 and SGS1 (for slow growth suppressor1), the sole budding yeast RecQ helicase homolog, the HR rate is higher than the rate of either single mutant, indicating two separate pathways with Mph1 and Sgs1 functioning in either one to suppress somatic HR (Schürer et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

The Fanconi Anemia Ortholog FANCM Ensures Ordered Homologous Recombination in Both Somatic and Meiotic Cells in Arabidopsis

et al. 2012

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The human hereditary disease Fanconi anemia leads to severe symptoms, including developmental defects and breakdown of the hematopoietic system. It is caused by single mutations in the FANC genes, one of which encodes the DNA translocase FANCM (for Fanconi anemia complementation group M), which is required for the repair of DNA interstrand cross-links to ensure replication progression. We identified a homolog of FANCM in Arabidopsis thaliana that is not directly involved in the repair of DNA lesions but suppresses spontaneous somatic homologous recombination via a RecQ helicase (At-RECQ4A)-independent pathway. In addition, it is required for double-strand break-induced homologous recombination. The fertility of Atfancm mutant plants is compromised. Evidence suggests that during meiosis At-FANCM acts as antirecombinase to suppress ectopic recombination-dependent chromosome interactions, but this activity is antagonized by the ZMM pathway to enable the formation of interference-sensitive crossovers and chromosome synapsis. Surprisingly, mutation of At-FANCM overcomes the sterility phenotype of an At-MutS homolog4 mutant by apparently rescuing a proportion of crossover-designated recombination intermediates via a route that is likely At-MMS and UV sensitive81 dependent. However, this is insufficient to ensure the formation of an obligate crossover. Thus, At-FANCM is not only a safeguard for genome stability in somatic cells but is an important factor in the control of meiotic crossover formation.

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Budding yeast Mph1 promotes sister chromatid interactions by a mechanism involving strand invasion

Cited by 10 publications

References 83 publications

Interactions of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae

Interactions of the HSM3 gene with genes initiating homologous recombination repair in yeast Saccharomyces cerevisiae

Functions and regulation of the multitasking FANCM family of DNA motor proteins

The Fanconi Anemia Ortholog FANCM Ensures Ordered Homologous Recombination in Both Somatic and Meiotic Cells in Arabidopsis

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