DNA methylation in imprinted genes IGF2 and GNASXL is associated with prenatal maternal stress

2015 ◽  
Vol 61 ◽  
pp. 16 ◽  
Author(s):  
Elise Beau Vangeel ◽  
Benedetta Izzi ◽  
Titia Hompes ◽  
Kristof Vansteelandt ◽  
Diether Lambrechts ◽  
...  
Epigenetics ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. 749-761 ◽  
Author(s):  
Lei Cao-Lei ◽  
Kelsey N Dancause ◽  
Guillaume Elgbeili ◽  
Renaud Massart ◽  
Moshe Szyf ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107653 ◽  
Author(s):  
Lei Cao-Lei ◽  
Renaud Massart ◽  
Matthew J. Suderman ◽  
Ziv Machnes ◽  
Guillaume Elgbeili ◽  
...  

2015 ◽  
Vol 14 (8) ◽  
pp. 573-582 ◽  
Author(s):  
E. B. Vangeel ◽  
B. Izzi ◽  
T. Hompes ◽  
K. Vansteelandt ◽  
D. Lambrechts ◽  
...  

2012 ◽  
Vol 41 (5) ◽  
pp. 609-626 ◽  
Author(s):  
Dawn Kingston ◽  
Wendy Sword ◽  
Paul Krueger ◽  
Steve Hanna ◽  
Maureen Markle‐Reid

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Anne-Marie Turcotte-Tremblay ◽  
Robert Lim ◽  
David P. Laplante ◽  
Lester Kobzik ◽  
Alain Brunet ◽  
...  

Little is known about how prenatal maternal stress (PNMS) influences risks of asthma in humans. In this small study, we sought to determine whether disaster-related PNMS would predict asthma risk in children. In June 1998, we assessed severity of objective hardship and subjective distress in women pregnant during the January 1998 Quebec Ice Storm. Lifetime asthma symptoms, diagnoses, and corticosteroid utilization were assessed when the children were 12 years old (N=68). No effects of objective hardship or timing of the exposure were found. However, we found that, in girls only, higher levels of prenatal maternal subjective distress predicted greater lifetime risk of wheezing (OR=1.11; 90% CI = 1.01–1.23), doctor-diagnosed asthma (OR=1.09; 90% CI = 1.00–1.19), and lifetime utilization of corticosteroids (OR=1.12; 90% CI = 1.01–1.25). Other perinatal and current maternal life events were also associated with asthma outcomes. Findings suggest that stress during pregnancy opens a window for fetal programming of immune functioning. A sex-based approach may be useful to examine how prenatal and postnatal environments combine to program the immune system. This small study needs to be replicated with a larger, more representative sample.


Reproduction ◽  
2010 ◽  
Vol 140 (3) ◽  
pp. 411-423 ◽  
Author(s):  
Philippe Arnaud

The cis-acting regulatory sequences of imprinted gene loci, called imprinting control regions (ICRs), acquire specific imprint marks in germ cells, including DNA methylation. These epigenetic imprints ensure that imprinted genes are expressed exclusively from either the paternal or the maternal allele in offspring. The last few years have witnessed a rapid increase in studies on how and when ICRs become marked by and subsequently maintain such epigenetic modifications. These novel findings are summarised in this review, which focuses on the germline acquisition of DNA methylation imprints and particularly on the combined role of primary sequence specificity, chromatin configuration, non-histone proteins and transcriptional events.


2021 ◽  
Vol 118 (5) ◽  
pp. e2005377118
Author(s):  
Weijun Jiang ◽  
Jiajia Shi ◽  
Jingjie Zhao ◽  
Qiu Wang ◽  
Dan Cong ◽  
...  

ZFP57 is a master regulator of genomic imprinting. It has both maternal and zygotic functions that are partially redundant in maintaining DNA methylation at some imprinting control regions (ICRs). In this study, we found that DNA methylation was lost at most known ICRs in Zfp57 mutant embryos. Furthermore, loss of ZFP57 caused loss of parent-of-origin–dependent monoallelic expression of the target imprinted genes. The allelic expression switch occurred in the ZFP57 target imprinted genes upon loss of differential DNA methylation at the ICRs in Zfp57 mutant embryos. Specifically, upon loss of ZFP57, the alleles of the imprinted genes located on the same chromosome with the originally methylated ICR switched their expression to mimic their counterparts on the other chromosome with unmethylated ICR. Consistent with our previous study, ZFP57 could regulate the NOTCH signaling pathway in mouse embryos by impacting allelic expression of a few regulators in the NOTCH pathway. In addition, the imprinted Dlk1 gene that has been implicated in the NOTCH pathway was significantly down-regulated in Zfp57 mutant embryos. Our allelic expression switch models apply to the examined target imprinted genes controlled by either maternally or paternally methylated ICRs. Our results support the view that ZFP57 controls imprinted expression of its target imprinted genes primarily through maintaining differential DNA methylation at the ICRs.


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