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XB-ART-57352
Birth Defects Res 2020 Nov 01;11219:1635-1659. doi: 10.1002/bdr2.1802.
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Role of epigenetics and miRNAs in orofacial clefts.

Garland MA , Sun B , Zhang S , Reynolds K , Ji Y , Zhou CJ .


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Orofacial clefts (OFCs) have multiple etiologies and likely result from an interplay between genetic and environmental factors. Within the last decade, studies have implicated specific epigenetic modifications and noncoding RNAs as additional facets of OFC etiology. Altered gene expression through DNA methylation and histone modification offer novel insights into how specific genes contribute to distinct OFC subtypes. Epigenetics research has also provided further evidence that cleft lip only (CLO) is a cleft subtype with distinct etiology. Polymorphisms or misexpression of genes encoding microRNAs, as well as their targets, contribute to OFC risk. The ability to experimentally manipulate epigenetic changes and noncoding RNAs in animal models, such as zebrafish, Xenopus, mice, and rats, has offered novel insights into the mechanisms of various OFC subtypes. Although much remains to be understood, recent advancements in our understanding of OFC etiology may advise future strategies of research and preventive care.

???displayArticle.pubmedLink??? 32926553
???displayArticle.pmcLink??? PMC7924905
???displayArticle.link??? Birth Defects Res
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Genes referenced: hdac3 hdac4 kdm6a phf8 prdm16 prmt1
GO keywords: DNA methylation [+]

???displayArticle.disOnts??? Wolf-Hirschhorn syndrome [+]
???displayArticle.omims??? KABUKI SYNDROME 1; KABUK1 [+]
References [+] :
Abbott, TCDD exposure of human embryonic palatal shelves in organ culture alters the differentiation of medial epithelial cells. 1991, Pubmed