Department of Cell Biology, Emory University School of Medicine, Atlanta GA 30322, USA.
Johns Hopkins University School of Medicine, Baltimore MD 21205, USA.
Development. 2021 Feb 10;148(3):dev196600. doi: 10.1242/dev.196600.
Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In , this reprogramming is mediated by the H3K4me2 demethylase SPR-5 and the H3K9 methyltransferase, MET-2. In contrast, the H3K36 methyltransferase MES-4 maintains H3K36me2/3 at germline genes between generations to facilitate re-establishment of the germline. To determine whether the MES-4 germline inheritance pathway antagonizes reprogramming, we examined the interaction between these two pathways. We found that the developmental delay of mutant progeny is associated with ectopic H3K36me3 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 MES-4 prevents crucial germline genes from being repressed by antagonizing maternal reprogramming. Thus, the balance of inherited histone modifications is necessary to distinguish germline versus soma and prevent developmental delay.This article has an associated 'The people behind the papers' interview.
受精卵的形成伴随着广泛的表观遗传重编程,以确保组蛋白甲基化的适当遗传,并防止发育迟缓。在这一过程中,H3K4me2 去甲基酶 SPR-5 和 H3K9 甲基转移酶 MET-2 介导了这一重编程。相比之下,H3K36 甲基转移酶 MES-4 在世代之间维持生殖系基因的 H3K36me2/3,以促进生殖系的重新建立。为了确定 MES-4 生殖系遗传途径是否拮抗重编程,我们研究了这两条途径之间的相互作用。我们发现, 突变体后代的发育迟缓与体细胞组织中 H3K36me3 的异位和 MES-4 靶向生殖系基因的异位表达有关。此外,这种发育迟缓依赖于 MES-4 和 H3K4 甲基转移酶 SET-2。我们提出,MES-4 通过拮抗母体重编程来防止关键的生殖系基因受到抑制。因此,遗传组蛋白修饰的平衡对于区分生殖系和体细胞以及防止发育迟缓是必要的。本文有一个相关的“论文背后的人物”采访。