AI Article Synopsis
- In somatic cells, DNA repair is reduced during mitosis to avoid issues like anaphase bridges, which can disrupt the separation of chromosomes.
- Research shows that while γH2AX signals (markers of DNA damage) linger in somatic cells, they peak and diminish quickly in mouse zygotes, suggesting their DNA repair process is effective even during mitosis.
- The lack of H2AX was found to improve the separation of sister chromatids and embryo development, indicating that the DNA repair system in zygotes is uniquely regulated to eliminate damaged cells and prevent mutation transmission to future generations.
Article Abstract
In somatic cells, DNA repair is attenuated during mitosis to prevent the formation of anaphase bridges and facilitate the proper segregation of sister chromatids. Irradiation-induced γH2AX foci persist for hours in M phase somatic cells. However, we observed that anaphase bridges formed in a significant fraction of mouse zygotes irradiated during mitosis. Additionally, γH2AX signals in M phase zygotes peaked 30 min after irradiation and subsequently reduced with a half-life within 1-2 h. These results suggest that the DNA repair system may operate efficiently in M phase zygotes following irradiation, leading to the frequent formation of anaphase bridges. The absence of H2AX promoted the successful segregation of sister chromatids and enhanced the development of embryos to the blastocyst stage. The DNA repair system may be differentially regulated during the M phase of the first cell cycle to ensure the immediate elimination of damaged zygotes, thereby efficiently preventing transmission of mutations to subsequent generations.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11153116 | PMC |
| http://dx.doi.org/10.1262/jrd.2024-018 | DOI Listing |
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