4.7 Article

Caenorhabditis elegans establishes germline versus soma by balancing inherited histone methylation

Journal

DEVELOPMENT
Volume 148, Issue 3, Pages -

Publisher

COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.196600

Keywords

Histone methylation; Developmental delay; Maternal reprogramming; Transgenerational inheritance; Epigenetics; Caenorhabditis elegans

Funding

  1. Division of Integrative Organismal Systems grant [NSF IOS1931697]
  2. National Institutes of Health Fellowships in Research and Science Teaching IRACDA postdoctoral program (NIH) [K12GM00680-15]
  3. National Institutes of Health (NIH) [F32 GM126734-01, F31 HD100145]

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The study demonstrates that in Caenorhabditis elegans, MES-4 protects key germline genes by preventing reprogramming, thus avoiding developmental delays.
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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