Caenorhabditis elegans establishes germline versus soma by balancing inherited histone methylation
Author(s) -
Brandon S. Carpenter,
Teresa W. Lee,
Caroline F. Plott,
Juan David González-Rodríguez,
Jovan S. Brockett,
Dexter A. Myrick,
David J. Katz
Publication year - 2021
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.196600
Subject(s) - biology , germline , reprogramming , caenorhabditis elegans , genetics , histone methylation , histone methyltransferase , epigenetics , demethylase , histone , somatic cell , ectopic expression , microbiology and biotechnology , dna methylation , gene , gene expression
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.
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