Overexpression of Snail family members highlights their ability to promote chick neural crest formation

Abstract

The Snail gene family of transcription factors plays crucial roles in different morphogenetic processes during the development of vertebrate and invertebrate embryos. In previous studies of function interference for one of the family members, Slug, we showed its involvement and neural crest formation in the chick embryo. Now we have carried out a series of gain-of-function experiments in which we show that Slug overexpression in the neural tube of the chick embryo induces an increase in neural crest production. The analysis of electroporated embryos shows that Slug can induce the expression of rhoB and an increase in the number of HNK-1-positive migratory cells, indicating that it lies upstream of them in the genetic cascade of neural crest development. The increase in neural crest production after Slug overexpression was confined to the cranial region, indicating that the mechanisms of crest induction somehow differ between head and trunk. The expression of the two vertebrate family members, Slug and Snail, is peculiar with respect to the neural crest. Slug is not expressed in the premigratory crest in the mouse, whereas it is expressed in this cell population in the chick and the opposite is true for Snail(Sefton, M., Sánchez, S. and Nieto M. A. (1998) Development125, 3111-3121). This raises the question of whether they can be functionally equivalent. To test this hypothesis both intra- and interspecies, we have performed a series of ectopic expression experiments by electroporating chick and mouse Snail in the chick embryo hindbrain. We observe that both genes elicit the same responses in the neural tube. Our results indicate that they can be functionally equivalent, although the embryos show a higher response to the endogenous gene, chick Slug.

Evidence That Tumor Microenvironment Initiates Epithelial-To-Mesenchymal Transition and Calebin A can Suppress it in Colorectal Cancer Cells

“…Among the epigenetic and genetic modifications, excessive methylation of the E-cadherin promoter and transcriptional suppression are observed as major activities in most carcinomas (Yoshiura et al, 1995;Tamura et al, 2000;Cheng et al, 2001;Hajra et al, 2002). In addition, transcriptional repressors of the Snail zinc finger transcription factor family, such as Snail and Slug, play an essential role in the activation and induction of EMT, as this alters the expression patterns of EMT biomarkers in favor of the mesenchymal phenotype (LaBonne and Bronner-Fraser, 2000;del Barrio and Nieto, 2002;Nieto, 2002). Indeed, the inflammatory TME has been further shown to induce cancer initiation, and metastasis through stimulating the EMT process (Buhrmann et al, 2016).…”

FGF8 signaling sustains progenitor status and multipotency of cranial neural crest-derived mesenchymal cellsin vivoandin vitro

“…Although CNC cells are a multi-potent cell population, they are usually regarded as progenitors but not stem cells due to their limited developmental potential, despite the existence of a small portion of multi-potent cells (Baroffio et al, 1991;Morrison et al, 1999;Crane and Trainor, 2006). Whether the fates of CNC cells are determined before or after migration remains in debate (Noden, 1983;del Barrio and Nieto, 2002;Trainor et al, 2002). It was reported previously that the mouse odontogenic CNC cells migrate into the first pharyngeal arch only at the 10-12 somite stage, suggesting that the odontogenic progenitors are committed during the pre-migratory or migrating stages (Zhang et al, 2003).…”

16p12.1 Deletion Orthologs are Expressed in Motile Neural Crest Cells and are Important for Regulating Craniofacial Development in Xenopus laevis

“…The process of NCC induction and specification is complex and requires a specific level of signaling by the BMP, Wnt, FGF, RA, Shh, and Notch/Delta pathways to establish a gene regulatory network that is crucial for determining NCC identity ( Villanueva et al, 2002 ; Monsoro-Burq et al, 2003 ; Wu et al, 2005 ; Theveneau and Mayor, 2012 ; Pla and Monsoro-Burq, 2018 ; Rogers and Nie, 2018 ; Prasad et al, 2019 ). During the early steps of NCC formation, these morphogen pathways work in concert with various NCC transcription factors (TFs) such as snai1 , snai2/slug , sox9 , and twist , to establish the neural plate border, regulate NCC specification, and subsequent NCC migration ( Aybar et al, 2003 ; del Barrio and Nieto, 2002 ; LaBonne and Bronner-Fraser, 1998 , 2000 ; Pla and Monsoro-Burq, 2018 ; Rogers and Nie, 2018 ; Spokony et al, 2002 ). As shown in the previous sections, we found that partial depletion of several 16p12.1-affected genes significantly impacted twist expression patterns and NCC migration in the PAs, and that these defects were not due to changes in NCC proliferation rates.…”