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Genome-wide disruption of DNA methylation by 5-aza-2'-deoxycytidine in the parasitoid wasp Nasonia vitripennis

Nicola Cook, View ORCID ProfileDarren J Parker, Frances Turner, Eran Tauber, Bart A Pannebakker, David M Shuker
doi: https://doi.org/10.1101/437202
Nicola Cook
School of Biology, University of St Andrews, UK;
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Darren J Parker
Department of Ecology and Evolution, University of Lausanne, Switzerland;
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  • ORCID record for Darren J Parker
Frances Turner
Edinburgh Genomics, School of Biological Sciences, University of Edinburgh, UK;
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Eran Tauber
Faculty of Natural Sciences, University of Haifa, Israel;
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Bart A Pannebakker
Laboratory of Genetics, Wageningen University, The Netherlands
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David M Shuker
School of Biology, University of St Andrews, UK;
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  • For correspondence: dms14@st-andrews.ac.uk
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Abstract

DNA methylation of cytosine residues across the genome influences how genes and phenotypes are regulated in a wide range of organisms. As such, understanding the role of DNA methylation and other epigenetic mechanisms has become very much a part of mapping genotype to phenotype, a major question in evolutionary biology. Ideally, we would like to manipulate DNA methylation patterns on a genome-wide scale, to help us to elucidate the role that epigenetic modifications play in phenotypic expression. Recently, the demethylating agent 5-aza-2'-deoxycytidine (5-aza-dC; commonly used in the epigenetic treatment of certain cancers), has been deployed to explore the epigenetic regulation of a number of traits of interest to evolutionary ecologists, including facultative sex allocation in the parasitoid wasp Nasonia vitripennis. In a recent study, we showed that treatment with 5-aza-dC did not ablate the facultative sex allocation response in Nasonia, but shifted the patterns of sex allocation in a way predicted by genomic conflict theory. This was the first (albeit indirect) experimental evidence for genomic conflict over sex allocation facilitated by DNA methylation. However, that work lacked direct evidence of the effects of 5-aza-dC on DNA methylation, and indeed the effect of the chemical has since been questioned in Nasonia. Here, using whole-genome bisulphite sequencing of more than 4 million CpGs, across more than 11,000 genes, we demonstrate unequivocally that 5-aza-dC disrupts methylation on a large scale across the Nasonia vitripennis genome. We show that the disruption can lead to both hypo- and hyper-methylation, may vary across tissues and time of sampling, and that the effects of 5-aza-dC are context- and sequence specific. We conclude that 5-aza-dC does indeed have the potential to be repurposed as a tool for studying the role of DNA methylation in evolutionary ecology, whilst many details of its action remain to be discovered.

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  • Typo in title!

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted October 09, 2018.
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Genome-wide disruption of DNA methylation by 5-aza-2'-deoxycytidine in the parasitoid wasp Nasonia vitripennis
Nicola Cook, Darren J Parker, Frances Turner, Eran Tauber, Bart A Pannebakker, David M Shuker
bioRxiv 437202; doi: https://doi.org/10.1101/437202
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Genome-wide disruption of DNA methylation by 5-aza-2'-deoxycytidine in the parasitoid wasp Nasonia vitripennis
Nicola Cook, Darren J Parker, Frances Turner, Eran Tauber, Bart A Pannebakker, David M Shuker
bioRxiv 437202; doi: https://doi.org/10.1101/437202

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