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Genetic and Epigenetic Regulation of Zebrafish Intestinal Development

1
Department Molecular Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Centre, 6525 GA Nijmegen, The Netherlands
2
Department Molecular Biology, Radboud Institute for Molecular Life Sciences, Faculty of Science, Radboud University, 6525 GA Nijmegen, The Netherlands
3
Institute for Environmental Studies, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands
*
Author to whom correspondence should be addressed.
Current address: Department of Pediatric Oncology, Hematology, and Clinical Immunology, University Hospital Düsseldorf, 40225 Düsseldorf, Germany.
Current address: Institute for Risk Assessment Sciences, Utrecht University, 3584 CM Utrecht, The Netherlands.
Epigenomes 2018, 2(4), 19; https://doi.org/10.3390/epigenomes2040019
Received: 23 August 2018 / Revised: 17 October 2018 / Accepted: 18 October 2018 / Published: 23 October 2018
(This article belongs to the Special Issue Polycomb and Trithorax Group of Proteins in Development and Disease)
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Abstract

Many regulatory pathways are conserved in the zebrafish intestine compared to mammals, rendering it a strong model to study intestinal development. However, the (epi)genetic regulation of zebrafish intestinal development remains largely uncharacterized. We performed RNA-sequencing and chromatin immunoprecipitation (ChIP)-sequencing for activating (H3K4me3) and repressive (H3K27me3) chromatin marks on isolated intestines at 5, 7, and 9 days post-fertilization (dpf), during which zebrafish transit from yolk dependence to external feeding. RNA-sequencing showed the enrichment of metabolic maintenance genes at all time points and a significant increase in lipid metabolism between 5 and 9 dpf. A strong correlation was observed between gene expression and presence of chromatin marks on gene promoters; H3K4me3-marked genes were expressed higher than H3K27m3-marked genes. Next, we studied a key epigenetic player, Enhancer of zeste homolog 2 (Ezh2). Ezh2 places the repressive H3K27me3 mark on the genome and is highly conserved in vertebrates. We used the nonsense mutant allele ezh2(hu5670) to study the effect of ezh2 loss on intestinal development. These mutants survived gastrulation and died around 11 dpf, showing severe morphological defects in the intestine and liver, accompanied by decreased intestinal (fabp2) and hepatic (fabp10a) marker expressions. Our results suggest that Ezh2 is essential for proper intestinal tissue maintenance and overall survival. View Full-Text
Keywords: zebrafish; development; ENU mutagenesis; Polycomb repressive complex 2; gene expression; transcriptomics; epigenetics; Ezh2 zebrafish; development; ENU mutagenesis; Polycomb repressive complex 2; gene expression; transcriptomics; epigenetics; Ezh2
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San, B.; Aben, M.; Elurbe, D.M.; Voeltzke, K.; Den Broeder, M.J.; Rougeot, J.; Legler, J.; Kamminga, L.M. Genetic and Epigenetic Regulation of Zebrafish Intestinal Development. Epigenomes 2018, 2, 19.

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