Yuan WANG, Dai TSUKIOKA, Shoji ODA, Hiroshi MITANI, Fugaku AOKI
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引用次数: 0
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.
在体细胞中,DNA修复在有丝分裂过程中会减弱,以防止无丝分裂桥的形成,并促进姐妹染色单体的正确分离。在 M 期体细胞中,辐照诱导的 γH2AX 病灶可持续数小时。然而,我们观察到,在有丝分裂过程中接受辐照的小鼠合子中有相当一部分形成了无丝分裂桥。这些结果表明,DNA修复系统可能在辐照后的M期子代中有效运作,从而导致无丝分裂桥的频繁形成。H2AX 的缺失促进了姐妹染色单体的成功分离,并使胚胎发育到囊胚阶段。在第一个细胞周期的 M 期,DNA 修复系统可能受到不同程度的调控,以确保立即消除受损的子染色体,从而有效地防止突变传给后代。
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