MORC1 represses transposable elements in the mouse male germ line

The Microrchidia (Morc) family of GHKL ATPases are present in a wide variety of prokaryotic and eukaryotic organisms but are of largely unknown function. Genetic screens in Arabidopsis thaliana have identified Morc genes as important repressors of transposons and other DNA methylated and silent genes. MORC1 deficient mice were previously found to display male-specific germ cell loss and infertility. Here we show that MORC1 is responsible for transposon repression in the male germline in a pattern that is similar to that observed for germ cells deficient for the DNA methyltransferase homolog DNMT3L. Morc1 mutants show highly localized defects in the establishment of DNA methylation at specific classes of transposons, and this is associated with failed transposon silencing at these sites. Our results identify MORC1 as an important new regulator of the epigenetic landscape of male germ cells during the period of global de novo methylation. This data includes: 47 RNA-seq, 4 smRNA-seq, 6 BS-seq, and 2 ChIP-seq datasetsMicrorchidia（Morc）家族属于GHKL ATP酶（GHKL ATPase）家族，广泛分布于各类原核与真核生物中，但其功能大多尚未明确。在拟南芥（Arabidopsis thaliana）中开展的遗传筛选已证实，Morc基因是转座子（transposon）及其他DNA甲基化沉默基因的重要抑制因子。此前的研究发现，MORC1缺陷型小鼠会出现雄性特异性生殖细胞缺失与不育表型。本研究证实，MORC1在雄性生殖系中负责转座子抑制，其调控模式与DNA甲基转移酶同源物DNMT3L（DNA methyltransferase homolog DNMT3L）缺陷型生殖细胞中观察到的模式相似。Morc1突变体在特定类别转座子的DNA甲基化建立过程中呈现高度局域化的缺陷，这与这些位点的转座子沉默失效密切相关。本研究结果表明，MORC1是雄性生殖细胞在全局从头甲基化阶段表观遗传图谱的重要新型调控因子。本数据集包含47份RNA测序（RNA-seq）、4份小RNA测序（smRNA-seq）、6份亚硫酸氢盐测序（BS-seq）以及2份染色质免疫共沉淀测序（ChIP-seq）数据集。