The molecular mechanism underlying epigenetic inheritance remains largely unknown. Previous studies have shown that transmission of paternally acquired traits through the male germline (i.e., sperm) requires functional DNMT2 to maintain normal profiles of sperm-borne tRNA-derived small RNAs (tsRNAs). Here we report that maternal transmission of a Kit paramutant phenotype (white tail tip) through the female germline (i.e., oocytes) also requires normal function of DNMT2 and normal profiles of DNMT2-dependent tsRNAs and other small noncoding RNAs (sncRNAs) in sperm. Specifically, the ablation of DNMT2 leads to aberrant profiles of tsRNAs and other sncRNAs in sperm, which correlate with drastically dysregulated mRNA transcriptome in pronuclear zygotes derived from oocytes carrying the Kit paramutation and a complete blockage of transmission of the paramutant phenotype through the oocytes. Together with previous reports, the present study suggests that both paternal and maternal transmission of epigenetic phenotypes requires DNMT2-dependent tsRNAs in sperm.

中文翻译：

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母源传递的突变体表型需要雄性种系中完整的DNMT2功能

表观遗传遗传的分子机制仍是未知之数。先前的研究表明，通过雄性种系（即精子）传播父系获得的性状需要功能性DNMT2来维持精子携带的tRNA衍生的小RNA（tsRNA）的正常特性。在这里我们报告说，通过女性生殖系（即卵母细胞）的Kit突变体表型（白色尾尖）的母体传播也需要DNMT2的正常功能以及DNMT2依赖的tsRNA和精子中其他小非编码RNA（sncRNA）的正常功能。具体而言，DNMT2的切除导致精子中tsRNA和其他sncRNA的异常概况，这与源自携带Kit突变的卵母细胞的原核受精卵中mRNA转录组的失调有关，并且完全阻断了该突变体表型通过卵母细胞的传递。与以前的报告一起，本研究表明表观遗传表型的父本和母本传播都需要精子中依赖DNMT2的tsRNA。