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. 2018 Mar 1;9:36. doi: 10.3389/fgene.2018.00036

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Copyright © 2018 de Sá Machado Araújo, da Silva Francisco Junior, dos Santos Ferreira, Mozer Rodrigues, Terra Machado, Louvain de Souza, Teixeira de Souza, Figueiredo Osorio da Silva, Alves da Silva, Andrade, da Silva, Ramos, Garcia, Machado and Medina-Acosta.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Absence of epipolymorphism at the PARD6G-AS1 and GCSAML maternal iDMRs in placentas from healthy and diseased pregnancies. The new maternal iDMRs are consistently hemimethylated in 450 K array (n = 90) methylomes from healthy; preeclampsia; and trisomy 13, 18, and 21 placentas. Comparison of the observed methylation levels in (A) the PARD6G-AS1 iDMR, (B) the PWWP2AP1 DMR, (C) the GCSAML iDMR, and (D) the WRB iDMR. Note that none of the conditions led to an unmethylated or hypermethylated status at the iDMRs. The hypomethylated status at the PARD6G-AS1 iDMR in some but not all trisomy 18 placentas suggests a paternal origin of the nondisjunction of the extra copy of chr18 in some placentas. The supernumerary chromosome 18 also perturbs the methylation status of the WRB iDMR in chromosome 21.