ArticleFrontiers in cell and developmental biology2026
Modelling DMC1 mediated homologous recombination repair in mouse embryonic stem cells.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Programmed DNA double-strand break (DSB) formation and repair are central to meiotic homologous chromosome pairing in mammals. In meiotic cells, the DSB repair mechanism is modified compared to mitotic cells to facilitate homologous chromosome pairing. Specifically, a subset of DSBs is repaired using the homologous chromosome rather than the sister chromatid as a repair template. How the ubiquitously expressed RAD51 and meiosis-specific DMC1 recombinases function together in this process in mammals is unknown. Methods: By ectopically expressing DMC1 in somatic mouse embryonic stem (mES) cells, and analyzing its effects on RAD51-dependent homologous recombination repair, we investigated DMC1-mediated mechanistic aspects of meiotic recombination without the need for mouse models or true in vitro gametogenesis. We used ionizing irradiation to induce DSBs, performed confocal and super-resolution microscopy to study recombinase localization dynamics and regulation of its recruitment. In addition, functional assays to assess homologous recombination activity, cell cycle and cell viability were performed in the presence and absence of DMC1. Results: First, we observed that, upon ectopic expression, DMC1 was recruited to irradiation-induced DSBs in mES cells. Interestingly, in addition to BRCA2, RAD51 loading was also critical for robust DMC1 recruitment to DSBs. After initial recruitment, we observed a gradual reduction in the number of DMC1 foci over time in both live and fixed mES cells. We also found that the presence of DMC1 had no adverse effect on cell cycle progression or mES cell viability. Finally, knock-in efficiency of DMC1 expressing cells was similar to that of control cells. Discussion: We show that the presence of DMC1 in mES cells allows progression of DSB repair in a manner similar to that seen in irradiated control cells. Furthermore, the results indicate that DMC1 and RAD51 most likely form productive structures to mediate repair, while the expression of DMC1 protein neither inhibits nor stimulates homologous recombination in this mES cell model.
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