Bani Ismail Mohammad, Shinohara Miki, Shinohara Akira
Institute for Protein Research, Graduate School of Science, Osaka University, Suita, Osaka, Japan.
PLoS One. 2014 May 5;9(5):e96648. doi: 10.1371/journal.pone.0096648. eCollection 2014.
Epigenetic marks such as histone modifications play roles in various chromosome dynamics in mitosis and meiosis. Methylation of histones H3 at positions K4 and K79 is involved in the initiation of recombination and the recombination checkpoint, respectively, during meiosis in the budding yeast. Set1 promotes H3K4 methylation while Dot1 promotes H3K79 methylation. In this study, we carried out detailed analyses of meiosis in mutants of the SET1 and DOT1 genes as well as methylation-defective mutants of histone H3. We confirmed the role of Set1-dependent H3K4 methylation in the formation of double-strand breaks (DSBs) in meiosis for the initiation of meiotic recombination, and we showed the involvement of Dot1 (H3K79 methylation) in DSB formation in the absence of Set1-dependent H3K4 methylation. In addition, we showed that the histone H3K4 methylation-defective mutants are defective in SC elongation, although they seem to have moderate reduction of DSBs. This suggests that high levels of DSBs mediated by histone H3K4 methylation promote SC elongation.
表观遗传标记,如组蛋白修饰,在有丝分裂和减数分裂的各种染色体动态变化中发挥作用。在芽殖酵母减数分裂过程中,组蛋白H3第4位赖氨酸(H3K4)和第79位赖氨酸(H3K79)的甲基化分别参与重组的起始和重组检查点。Set1促进H3K4甲基化,而Dot1促进H3K79甲基化。在本研究中,我们对SET1和DOT1基因的突变体以及组蛋白H3的甲基化缺陷突变体的减数分裂进行了详细分析。我们证实了Set1依赖的H3K4甲基化在减数分裂中双链断裂(DSB)形成以启动减数分裂重组中的作用,并且我们表明在不存在Set1依赖的H3K4甲基化的情况下,Dot1(H3K79甲基化)参与DSB形成。此外,我们表明组蛋白H3K4甲基化缺陷突变体在联会复合体(SC)延长方面存在缺陷,尽管它们似乎有适度减少的DSB。这表明由组蛋白H3K4甲基化介导的高水平DSB促进SC延长。