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DNA CpG methylation (5-methylcytosine) and its derivative (5-hydroxymethylcytosine) alter histone posttranslational modifications at the Pomc promoter, affecting the impact of perinatal diet on leanness and obesity of the offspring
Year:
2016
Source of publication :
Diabetes
Authors :
Kisliouk, Tatiana
;
.
Meiri, Noam
;
.
Volume :
65
Co-Authors:
Marco, A., Faculty of Life Sciences, Bar Ilan University, Ramat-Gan, Israel, Department of Psychology, Bar Ilan University, Ramat-Gan, Israel
Kisliouk, T., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Tabachnik, T., Faculty of Life Sciences, Bar Ilan University, Ramat-Gan, Israel, Department of Psychology, Bar Ilan University, Ramat-Gan, Israel
Weller, A., Department of Psychology, Bar Ilan University, Ramat-Gan, Israel, Gonda Multidisciplinary Brain Research Center, Bar Ilan University, Ramat-Gan, Israel
Meiri, N., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Facilitators :
From page:
2258
To page:
2267
(
Total pages:
10
)
Abstract:
A maternal high-fat diet (HFD) alters the offspring's feeding regulation, leading to obesity. This phenomenon is partially mediated by aberrant expression of the hypothalamic anorexigenic neuropeptide proopiomelanocortin (POMC). Nevertheless, although some individual offspring suffer from morbid obesity, others escape the malprogramming. It is suggested that this difference is due to epigenetic programming. In this study, we report that in lean offspring of non-HFD-fed dams, essential promoter regions for Pomc expression were enriched with 5-hydroxymethylcytosine (5hmC) together with a reduction in the level of 5-methylcytosine (5mC). Moreover, 5hmC was negatively correlated whereas 5mC was positively correlated with body weight in offspring from both HFD- and control-fed dams. We further found that Pomc expression in obese offspring is determined by a two-step epigenetic inhibitory mechanism in which CpG methylation is linked with histone posttranslational modifications. An increase in CpG methylation at the Poxmc promoter enables binding of methyl-binding domain 1 (MBD1) to 5mC, but not to its derivative 5hmC. MBD1 then interacts with SET domain bifurcated 1 methyltransferase to promote bimethylation on the histone 3 lysine 9 residue, reducing Pomc mRNA expression. These results suggest an epigenetic regulatory mechanism that affects obesity-prone or resilient traits. © 2016 by the American Diabetes Association.
Note:
Related Files :
epigenetics
Female
Gene
gene expression
methyl binding domain 1
obesity
perinatal period
Protein processing
Show More
Related Content
More details
DOI :
10.2337/db15-1608
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
31178
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 01:00
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Scientific Publication
DNA CpG methylation (5-methylcytosine) and its derivative (5-hydroxymethylcytosine) alter histone posttranslational modifications at the Pomc promoter, affecting the impact of perinatal diet on leanness and obesity of the offspring
65
Marco, A., Faculty of Life Sciences, Bar Ilan University, Ramat-Gan, Israel, Department of Psychology, Bar Ilan University, Ramat-Gan, Israel
Kisliouk, T., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Tabachnik, T., Faculty of Life Sciences, Bar Ilan University, Ramat-Gan, Israel, Department of Psychology, Bar Ilan University, Ramat-Gan, Israel
Weller, A., Department of Psychology, Bar Ilan University, Ramat-Gan, Israel, Gonda Multidisciplinary Brain Research Center, Bar Ilan University, Ramat-Gan, Israel
Meiri, N., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
DNA CpG methylation (5-methylcytosine) and its derivative (5-hydroxymethylcytosine) alter histone posttranslational modifications at the Pomc promoter, affecting the impact of perinatal diet on leanness and obesity of the offspring
A maternal high-fat diet (HFD) alters the offspring's feeding regulation, leading to obesity. This phenomenon is partially mediated by aberrant expression of the hypothalamic anorexigenic neuropeptide proopiomelanocortin (POMC). Nevertheless, although some individual offspring suffer from morbid obesity, others escape the malprogramming. It is suggested that this difference is due to epigenetic programming. In this study, we report that in lean offspring of non-HFD-fed dams, essential promoter regions for Pomc expression were enriched with 5-hydroxymethylcytosine (5hmC) together with a reduction in the level of 5-methylcytosine (5mC). Moreover, 5hmC was negatively correlated whereas 5mC was positively correlated with body weight in offspring from both HFD- and control-fed dams. We further found that Pomc expression in obese offspring is determined by a two-step epigenetic inhibitory mechanism in which CpG methylation is linked with histone posttranslational modifications. An increase in CpG methylation at the Poxmc promoter enables binding of methyl-binding domain 1 (MBD1) to 5mC, but not to its derivative 5hmC. MBD1 then interacts with SET domain bifurcated 1 methyltransferase to promote bimethylation on the histone 3 lysine 9 residue, reducing Pomc mRNA expression. These results suggest an epigenetic regulatory mechanism that affects obesity-prone or resilient traits. © 2016 by the American Diabetes Association.
Scientific Publication
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