Trans-generational epigenetic regulation of C. elegans primordial germ cells

• Type of Material: Article
• Authors: Hirofumi Furuhashi, Emory University; Teruaki Takasaki, University of California, Santa Cruz; Andreas Rechtsteiner, University of California, Santa Cruz; Tengguo Li, Emory University; Hiroshi Kimura, Osaka University; Paula M. Checchi, Emory University; Susan Strome, University of California, Santa Cruz; William G Kelly, Emory University
• Language: English
• Date: 2010-08-12
• Publisher: BioMed Central
• Publication Version: Final Published Version
• Copyright Statement: © 2010 Furuhashi et al; licensee BioMed Central Ltd.
• License: Creative Commons Attribution 2.0 Generic
• Final Published Version (URL): http://www.epigeneticsandchromatin.com/content/3/1/15
• Title of Journal or Parent Work: Epigenetics and Chromatin
• ISSN: 1756-8935
• Volume: 3
• Issue: 15
• Start Page: 1
• End Page: 21
• Grant/Funding Information: This work was supported by NIH grants GM077600 (W.G.K) and GM34059 (S.S.) and NHGRI modENCODE grant U01 HG004270.
• Research Categories: Biology, General; Biology, Genetics

Abstract

Background The processes through which the germline maintains its continuity across generations has long been the focus of biological research. Recent studies have suggested that germline continuity can involve epigenetic regulation, including regulation of histone modifications. However, it is not clear how histone modifications generated in one generation can influence the transcription program and development of germ cells of the next. Results We show that the histone H3K36 methyltransferase maternal effect sterile (MES)-4 is an epigenetic modifier that prevents aberrant transcription activity in Caenorhabditis elegans primordial germ cells (PGCs). In mes-4 mutant PGCs, RNA Pol II activation is abnormally regulated and the PGCs degenerate. Genetic and genomewide analyses of MES-4-mediated H3K36 methylation suggest that MES-4 activity can operate independently of ongoing transcription, and may be predominantly responsible for maintenance methylation of H3K36 in germline-expressed loci. Conclusions Our data suggest a model in which MES-4 helps to maintain an 'epigenetic memory' of transcription that occurred in germ cells of previous generations, and that MES-4 and its epigenetic product are essential for normal germ cell development.