| Literature DB >> 33462111 |
Brandon S Carpenter1, Teresa W Lee1, Caroline F Plott2, Juan D Rodriguez1, Jovan S Brockett3, Dexter A Myrick1, David J Katz4.
Abstract
Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In Caenorhabditis elegans, 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 spr-5; met-2 reprogramming, we examined the interaction between these two pathways. We found that the developmental delay of spr-5; met-2 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 spr-5; met-2 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.Entities:
Keywords: Caenorhabditis elegans; Developmental delay; Epigenetics; Histone methylation; Maternal reprogramming; Transgenerational inheritance
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Year: 2021 PMID: 33462111 PMCID: PMC7888751 DOI: 10.1242/dev.196600
Source DB: PubMed Journal: Development ISSN: 0950-1991 Impact factor: 6.862