Epigenetic landscape and miRNA involvement during neural crest development

Abstract

The neural crest (NC) is a multipotent, migratory cell population that arises from the dorsal neural fold of vertebrate embryos. NC cells migrate extensively and differentiate into a variety of tissues, including melanocytes, bone, and cartilage of the craniofacial skeleton, peripheral and enteric neurons, glia, and smooth muscle and endocrine cells. For several years, the gene regulatory network that orchestrates NC cells development has been extensively studied. However, we have recently begun to understand that epigenetic and posttranscriptional regulation, such as miRNAs, plays important roles in NC development. In this review, we focused on some of the most recent findings on chromatin-dependent mechanisms and miRNAs regulation during vertebrate NC cells development.

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

“…Several components of chromatin remodeling complexes, such as Brg1 and CHD7, have also been reported to influence neural crest induction and/or differentiation (Eroglu et al, 2006;Bajpai et al, 2010;Weider et al, 2012;Li et al, 2013). Furthermore, both microRNA-processing enzymes and several specific microRNAs have been shown to regulate neural crest migration or affect neural crest-derived tissues, such as cranial and cardiovascular structures (Prasad et al, 2012;Strobl-Mazzulla et al, 2012;Mayanil, 2013). A more recent report also indicates that Ezh2 is required for craniofacial skeleton development in mouse (Schwarz et al, 2014).…”

DNA methyltransferase 3B regulates duration of neural crest production via repression of Sox10

“…In addition to de novo DNA methytransferases, other epigenetic regulators, including histone demethylases and histone deacetylases, also have been shown to play a crucial role in regulating the timing of neural crest specification or migration (22,23). Histone demethylases, such as members of the Jumonji family, revert histone methylation (24).…”

Resolving Time and Space Constraints During Neural Crest Formation and Delamination

“…Contrary to miR-200s and miR-34, miR-9, which is upregulated in breast cancer cells and activated by Myc, has been found to directly target E-cadherin messages, leading to increased cell motility and invasiveness in epithelial cell lines (Ma et al, 2010). To date, the presence of these various miRNAs during specification and delamination of NCC has not been reported, yet, miRNAs undoubtedly play an important role in these cells (Mayanil, 2013;Strobl-Mazzulla, Marini, & Buzzi, 2012). Indeed, in mouse, specific deletion in NCC of DICER, the RNase III enzyme required for miRNAs maturation, leads to craniofacial and cardiac anomalies (Zehir, Hua, Maska, Morikawa, & Cserjesi, 2010).…”

“…Though still preliminary, recent studies have highlighted the major transcriptional reprogramming events that accompany NCC specification and delamination and provided insights into the synergistic control of NCC specifiers by the epigenetic machinery (Mayanil, 2013;Strobl-Mazzulla et al, 2012). DNA methylation by DNA-methyltransferases (DNMTs) is one of the epigenetic modifications resulting in transcriptional repression of genes.…”