DNA repair proteins can be recruited by their histone reader domains to specific epigenomic features, with consequences on intragenomic mutation rate variation. Here, we investigated H3K4me1-associated hypomutation in plants. We first examined two proteins which, in plants, contain Tudor histone reader domains: PRECOCIOUS DISSOCIATION OF SISTERS 5 (PDS5C), involved in homology-directed repair, and MUTS HOMOLOG 6 (MSH6), a mismatch repair protein. The MSH6 Tudor domain of Arabidopsis (Arabidopsis thaliana) binds to H3K4me1 as previously demonstrated for PDS5C, which localizes to H3K4me1-rich gene bodies and essential genes. Mutations revealed by ultradeep sequencing of wild-type and msh6 knockout lines in Arabidopsis show that functional MSH6 is critical for the reduced rate of single base substitution mutations in gene bodies and H3K4me1-rich regions. We explored the breadth of these mechanisms among plants by examining a large rice (Oryza sativa) mutation dataset. H3K4me1-associated hypomutation is conserved in rice as are the H3K4me1 binding residues of MSH6 and PDS5C Tudor domains. Recruitment of DNA repair proteins by H3K4me1 in plants reveals convergent, but distinct, epigenome-recruited DNA repair mechanisms from those well described in humans. The emergent model of H3K4me1-recruited repair in plants is consistent with evolutionary theory regarding mutation modifier systems and offers mechanistic insight into intragenomic mutation rate variation in plants.

中文翻译：

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H3K4me1 在植物中招募 DNA 修复蛋白

DNA 修复蛋白可以通过其组蛋白阅读器结构域招募到特定的表观基因组特征，从而对基因组内突变率变化产生影响。在这里，我们研究了植物中 H3K4me1 相关的低突变。我们首先检查了植物中含有 Tudor 组蛋白阅读器结构域的两种蛋白质：参与同源定向修复的早熟解离姐妹 5 (PDS5C) 和错配修复蛋白 MUTS HOMOLOG 6 (MSH6)。拟南芥 (Arabidopsis thaliana) 的 MSH6 Tudor 结构域与 H3K4me1 结合，正如之前针对 PDS5C 所证明的那样，PDS5C 定位于富含 H3K4me1 的基因体和必需基因。对拟南芥中野生型和 msh6 敲除品系的超深测序揭示的突变表明，功能性 MSH6 对于降低基因体和 H3K4me1 富含区域中单碱基取代突变率至关重要。我们通过检查大型水稻（Oryza sativa）突变数据集来探索植物中这些机制的广度。 H3K4me1 相关的低突变在水稻中是保守的，MSH6 和 PDS5C Tudor 结构域的 H3K4me1 结合残基也是如此。植物中 H3K4me1 招募 DNA 修复蛋白揭示了表观基因组招募的 DNA 修复机制与人类中所描述的机制趋同但又截然不同。植物中 H3K4me1 招募修复的新兴模型与突变修饰系统的进化理论一致，并为植物基因组内突变率变化提供了机制见解。