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Published on: June 25, 2013
Mnd1 is required for meiotic interhomolog repair
Christian Zierhut1, Marc Berlinger, Christian Rupp
1Max F. Perutz Laboratories, Cell Biology and Genetics, Institute of Botany, University of Vienna, Rennweg 14, A-1030, Vienna, Austria.
Background:
While double-strand break (DSB) repair is vital to the survival of cells during both meiosis and mitosis, the preferred mechanism of repair differs drastically between the two types of cell cycle. Thus, during meiosis, it is the homologous chromosome rather than the sister chromatid that is used as a repair template.
Results:
Cells attempting to undergo meiosis in the absence of Mnd1 arrest in prophase I due to the activation of the Mec1 DNA-damage checkpoint accumulating hyperresected DSBs and aberrant synapsis. Sporulation of mnd1Delta strains can be restored by deleting RED1 or HOP1, which permits repair of DSBs by using the sister chromatid as a repair template. Mnd1 localizes to chromatin as foci independently of DSB formation, axial element (AE) formation, and synaptonemal complex (SC) formation and does not colocalize with Rad51. Mnd1 does not preferentially associate with hotspots of recombination.
Conclusions:
Our results suggest that Mnd1 acts specifically to promote DSB repair by using the homologous chromosome as a repair template. The presence of Rec8, Red1, or Hop1 renders Mnd1 indispensable for DNA repair, presumably through the establishment of interhomolog (IH) bias. Localization studies suggest that Mnd1 carries out this function without being specifically recruited to the sites of DNA repair. We propose a model in which Mnd1 facilitates chromatin accessibility, which is required to allow strand invasion in meiotic chromatin.
Insights
Mnd1 protein is essential for homologous chromosome repair during meiosis. Its absence causes DNA damage arrest, but deleting other genes restores repair using sister chromatids.
Area of Science:
- Cellular and Molecular Biology
- Genetics and Genomics
- DNA Repair Mechanisms
Background:
- Double-strand break (DSB) repair is crucial for cell survival during meiosis and mitosis.
- Meiosis preferentially uses homologous chromosomes, not sister chromatids, as repair templates.
Purpose of the Study:
- To investigate the role of Mnd1 in meiotic double-strand break (DSB) repair.
- To understand the mechanism by which homologous chromosome repair is promoted during meiosis.
Main Methods:
- Analysis of meiotic progression in yeast strains with and without Mnd1.
- Genetic manipulation (deletions) to observe effects on DSB repair.
- Chromatin localization studies of Mnd1.
Main Results:
- Absence of Mnd1 leads to meiotic arrest in prophase I due to DNA damage checkpoint activation and DSB accumulation.
- Deleting RED1 or HOP1 in mnd1Δ strains restores sporulation by enabling sister chromatid repair.
- Mnd1 localizes to chromatin independently of DSB formation and recombination hotspots, and does not colocalize with Rad51.
Conclusions:
- Mnd1 specifically promotes DSB repair using the homologous chromosome as a template.
- Mnd1 is indispensable for DNA repair in the presence of Rec8, Red1, or Hop1, likely establishing interhomolog bias.
- Mnd1 may facilitate chromatin accessibility for strand invasion during meiotic repair without direct recruitment to DSB sites.
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