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Lookup NU author(s): Dr Louise Hyslop,
Professor Alison Murdoch,
Professor Miodrag Stojkovic,
Professor Mary Herbert
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It has long been appreciated that environmental cues may trigger adaptive responses. Many of these responses are a result of changes in the epigenetic landscape influencing transcriptional states and consequently altering phenotypes. In the context of human reproductive health, the procedures necessary for assisted reproduction may result in altered phenotypes by primarily influencing DNA methylation. Among the well-documented effects of assisted reproduction technologies (ART), imprinted genes appear to be frequently altered, likely owing to their reliance on DNA methylation to impose parent-specific monoallelic expression. However, the generality of the potential deregulation of DNA methylation in ART-derived human embryos has not been evaluated. In this study, we evaluate the genome-wide DNA methylation together with chromatin organisation in human embryos derived by either IVF (n = 89) or ICSI (n = 76). DNA methylation was assessed using an antibody against 5-methyl-cytidine, and chromatin organisation by DNA staining. Irrespective of the ART procedure, similar errors were observed in both groups and abnormal chromatin was positively correlated (P < 0.001) with inappropriate DNA methylation. Development up to the blastocyst stage was consistent with normal DNA methylation and chromatin organisation, reinforcing the importance of epigenetic regulation to form the early lineages of the blastocyst. Most importantly, we found no evidence that ICSI blastocysts were more severely affected than those derived by IVF. We conclude that ICSI does not lead to an increased incidence of epigenetic errors (DNA methylation and chromatin) compared with IVF.
Author(s): Santos F, Hyslop L, Stojkovic P, Leary C, Murdoch A, Reik W, Stojkovic M, Herbert M, Dean W
Publication type: Article
Publication status: Published
Journal: Human Reproduction
Print publication date: 15/07/2010
ISSN (print): 0268-1161
ISSN (electronic): 1460-2350
Publisher: Oxford University Press
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