Embryos undergo extensive reprogramming at fertilization to prevent the inappropriate inheritance of histone methylation. In C. elegans, this reprogramming is mediated by the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2. In contrast to this reprogramming, the H3K36 methyltransferase, MES-4, maintains H3K36me2/3 at germline genes between generations to help re-establish the germline. To determine whether the MES-4 germline inheritance system antagonizes spr-5; met-2 reprogramming, we examined the interaction between these two systems. We find that the developmental delay of spr-5; met-2 mutant progeny is associated with ectopic H3K36me2/3 and the ectopic expression of MES-4 targeted germline genes in somatic tissues. Furthermore, the developmental delay is dependent upon MES-4 and the H3K4 methyltransferase, SET-2. We propose that the MES-4 inheritance system prevents critical germline genes from being repressed by maternal spr-5; met-2 reprogramming. Thus, the balance of inherited histone modifications is necessary to distinguish germline versus soma and prevent developmental delay.

中文翻译：

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秀丽隐杆线虫通过平衡遗传的组蛋白甲基化来建立种系与体细胞

胚胎在受精时要进行大量的重新编程，以防止组蛋白甲基化的不当遗传。在秀丽隐杆线虫中，这种重编程由H3K4me2脱甲基酶SPR-5和H3K9甲基转移酶MET-2介导。与这种重新编程相反，H3K36甲基转移酶MES-4在世代之间的种系基因上维持H3K36me2 / 3，以帮助重新建立种系。确定MES-4种系遗传系统是否拮抗spr-5；met-2重新编程，我们检查了这两个系统之间的交互。我们发现spr-5的发育延迟；met-2突变子代与异位H3K36me2 / 3和MES-4靶向种系基因在体细胞组织中的异位表达有关。此外，发育延迟取决于MES-4和H3K4甲基转移酶SET-2。我们建议，MES-4遗传系统可以防止关键的种系基因受到母体spr-5的抑制。met-2重新编程。因此，遗传组蛋白修饰的平衡对于区分种系与体细胞以及防止发育延迟是必要的。