Key Laboratory of Epigenetic Regulation and Intervention, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai 200031, China.
CAS Key Laboratory of Computational Biology, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai 200031, China.
Sci Adv. 2024 Oct 11;10(41):eadr2345. doi: 10.1126/sciadv.adr2345. Epub 2024 Oct 9.
Meiotic recombination between homologous chromosomes is vital for maximizing genetic variation among offspring. However, sex-determining regions are often rearranged and blocked from recombination. It remains unclear whether rearrangements or other mechanisms might be responsible for recombination suppression. Here, we uncover that the deficiency of the DNA cytosine methyltransferase DNMT1 in the green alga causes anomalous meiotic recombination at the mating-type locus (), generating haploid progeny containing both and mating-type markers due to crossovers within . The deficiency of a histone methyltransferase for H3K9 methylation does not lead to anomalous recombination. These findings suggest that DNA methylation, rather than rearrangements or histone methylation, suppresses meiotic recombination, revealing an unappreciated biological function for DNA methylation in eukaryotes.
减数分裂过程中同源染色体间的重组对于最大化后代的遗传多样性至关重要。然而，性决定区域经常发生重排并被阻止重组。目前尚不清楚是重排还是其他机制导致了重组的抑制。在这里，我们发现绿色藻类中的 DNA 胞嘧啶甲基转移酶 DNMT1 的缺陷导致了交配型基因座（）处异常的减数分裂重组，由于在 内发生了交叉，产生了含有 和 交配型标记的单倍体后代。组蛋白 H3K9 甲基转移酶的缺陷不会导致异常重组。这些发现表明，DNA 甲基化而不是重排或组蛋白甲基化抑制了减数分裂重组，揭示了 DNA 甲基化在真核生物中一个未被充分认识的生物学功能。
