Epigenetic regulation in neural crest development

Liu, Yifei; Xiao, Andrew

doi:10.1002/bdra.20797

Cited by 15 publications

(11 citation statements)

References 125 publications

(121 reference statements)

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“…Several distinct epigenetic programs, including histone modification, chromatin remodeling and non-coding RNA (e.g. miRNAs), have been implicated in different steps of neural crest development in various species (Liu and Xiao, 2011;Prasad et al, 2012;StroblMazzulla et al, 2012;Mayanil, 2013). For example, it has been shown that the histone H3K9me3/H3K36me3 demethylase JmjD2A regulates neural crest specification in the chick (StroblMazzulla et al, 2010), and the PRC1 component Ring1b specifically modulates craniofacial chondrocyte differentiation in zebrafish without affecting early induction and migration of the neural crest (van der Velden et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Snail2/Slug cooperates with Polycomb repressive complex 2 (PRC2) to regulate neural crest development

et al. 2015

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Neural crest cells arise from the border of the neural plate and epidermal ectoderm, migrate extensively and differentiate into diverse cell types during vertebrate embryogenesis. Although much has been learnt about growth factor signals and gene regulatory networks that regulate neural crest development, limited information is available on how epigenetic mechanisms control this process. In this study, we show that Polycomb repressive complex 2 (PRC2) cooperates with the transcription factor Snail2/Slug to modulate neural crest development in Xenopus. The PRC2 core components Eed, Ezh2 and Suz12 are expressed in the neural crest cells and are required for neural crest marker expression. Knockdown of Ezh2, the catalytic subunit of PRC2 for histone H3K27 methylation, results in defects in neural crest specification, migration and craniofacial cartilage formation. EZH2 interacts directly with Snail2, and Snail2 fails to expand the neural crest domains in the absence of Ezh2. Chromatin immunoprecipitation analysis shows that Snail2 regulates EZH2 occupancy and histone H3K27 trimethylation levels at the promoter region of the Snail2 target E-cadherin. Our results indicate that Snail2 cooperates with EZH2 and PRC2 to control expression of the genes important for neural crest specification and migration during neural crest development.

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Section: Discussionmentioning

confidence: 99%

Snail2/Slug cooperates with Polycomb repressive complex 2 (PRC2) to regulate neural crest development

et al. 2015

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“…The epigenetic machinery falls into the following groups: DNA methylation, histone methylation, histone acetylation, Polycomb repressive complex, ATP-dependent chromatin remodeling complex, and other regulators that work with the epigenetic machinery to regulate neural crest development. Different types of DNA and histone modifications and family members of chromatin remodeling complexes have been reviewed recently in (Liu and Xiao, 2011). …”

Section: Overview Of Epigenetic Regulationmentioning

confidence: 99%

Epigenetic regulation in neural crest development

Strobl-Mazzulla

Bronner‐Fraser

2014

Developmental Biology

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The neural crest is a migratory and multipotent cell population that plays a crucial many aspects of embryonic development. In all vertebrate embryos, these cells emerge from the dorsal neural tube then migrate long distances to different regions of the body, where they contribute to formation of many cell types and structures. These include much of the peripheral nervous system, craniofacial skeleton, smooth muscle, and pigmentation of the skin. The best-studied regulatory events guiding neural crest development are mediated by transcription factors and signaling molecules. In recent years, however, growing evidence supports an important role for epigenetic regulation as an additional mechanism for controlling the timing and level of gene expression at different stages of neural crest development. Here, we summarize the process of neural crest formation, with focus on the role of epigenetic regulation in neural crest specification, migration, and differentiation as well as in neural crest related birth defects and diseases.

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“…Second, folate and methyl donors provide methyl groups for DNA and protein methylation (47,51). Given the increasing attention to the role of epigenetics in NCC regulation and action (52), it is conceivable that the protective action of dietary methyl donors is through facilitation of epigenetic gene regulation in NCCs of BA1. This idea is supported by the observation that the supplemented diet used in this study is able to alter DNA methylation status and gene regulation at epigenetically labile loci, such as those in the agouti viable yellow (40)(41)(42) and axin fused (53) strains.…”

Section: Discussionmentioning

confidence: 99%

Maternal Diet Supplementation with Methyl Donors and Increased Parity Affect the Incidence of Craniofacial Defects in the Offspring of Twisted gastrulation Mutant Mice

Billington

Schmidt

Zhang

et al. 2013

The Journal of Nutrition

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Diets rich in methyl-donating compounds, including folate, can provide protection against neural tube defects, but their role in preventing craniofacial defects is less clear. Mice deficient in Twisted gastrulation (TWSG1), an extracellular modulator of bone morphogenetic protein signaling, manifest both midline facial defects and jaw defects, allowing study of the effects of methyl donors on various craniofacial defects in an experimentally tractable animal model. The goal of this study was to examine the effects of maternal dietary supplementation with methyl donors on the incidence and type of craniofacial defects among Twsg1 2/2 offspring. Nulliparous and primiparous female mice were fed an NIH31 standard diet (control) or a methyl donor supplemented (MDS) diet (folate, vitamin B-12, betaine, and choline). Observed defects in the pups were divided into those derived mostly from the first branchial arch (BA1) (micrognathia, agnathia, cleft palate) and midline facial defects in the holoprosencephaly spectrum (cyclopia, proboscis, and anterior truncation). In the first pregnancy, offspring of mice fed the MDS diet had lower incidence of BA1-derived defects (12.8% in MDS vs. 32.5% in control; P = 0.02) but similar incidence of midline facial defects (6.4% in MDS vs. 5.2% in control; P = 1.0). Increased maternal parity was independently associated with increased incidence of craniofacial defects after adjusting for diet (from 37.7 to 59.5% in control, P = 0.04 and from 19.1 to 45.3% in MDS, P = 0.045). In conclusion, methyl donor supplementation shows protective effects against jaw defects, but not midline facial defects, and increased parity can be a risk factor for some craniofacial defects.

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Epigenetic regulation in neural crest development

Cited by 15 publications

References 125 publications

Snail2/Slug cooperates with Polycomb repressive complex 2 (PRC2) to regulate neural crest development

Snail2/Slug cooperates with Polycomb repressive complex 2 (PRC2) to regulate neural crest development

Epigenetic regulation in neural crest development

Maternal Diet Supplementation with Methyl Donors and Increased Parity Affect the Incidence of Craniofacial Defects in the Offspring of Twisted gastrulation Mutant Mice

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