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This article is part of the supplement: Epigenetics and Chromatin: Interactions and processes

Open Access Oral presentation

Germline epigenetics, and reprogramming in zebrafish early embryos

Magdalena E Potok, David A Nix, Timothy J Parnell and Bradley R Cairns*

  • * Corresponding author: Bradley R Cairns

Author Affiliations

Howard Hughes Medical Institute, Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT 84112, USA

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Epigenetics & Chromatin 2013, 6(Suppl 1):O23  doi:10.1186/1756-8935-6-S1-O23


The electronic version of this article is the complete one and can be found online at: http://www.epigeneticsandchromatin.com/content/6/S1/O23


Published:18 March 2013

© 2013 Potok et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Oral presentation

Early vertebrate embryos must achieve totipotency and prepare for zygotic genome activation (ZGA). To better understand, we determined DNAme profiles of zebrafish gametes, multiple embryo stages flanking ZGA, and somatic muscle - and compared them to gene activity and histone modifications. First, sperm chromatin patterns are virtually identical to those at ZGA. Unexpectedly, in the oocyte many genes important for germline functions (ie. piwil1) or early development (ie. hox genes) are DNA methylated - yet demethylated during zygotic/cleavage stages to precisely the state observed in sperm. Remarkably, this cohort constitutes the genes/loci that acquire DNAme during development (ie. ZGA to muscle). Furthermore, DNA methyltransferase inhibition experiments suggests that DNAme silences particular gene/chromatin cohorts at ZGA, preventing their precocious expression. Thus, zebrafish appear to achieve a 'totipotent' chromatin state at ZGA through paternal genome competency, maternal genome DNA demethylation/reprogramming, and the imposition of DNA methylation on genes needed later in development.