Expression of Xenopus snail in mesoderm and prospective neural fold ectoderm

Abstract

Expression of the Xsna gene during Xenopus laevis embryogenesis has been analysed by in situ hybridisation. Like its homol o p e snail in Drosophila, Xsna is expressed zygotically in all early mesoderm. Expression starts during stage 9 in the dorsal marginal zone and spreads to the ventral side by stage 10. During gastrulation, each cell begins to express as it involutes so that cells newly expressing Xsna are added to the forming mesoderm mantle in an anterior-to-posterior progression. Xsna expression is then down-regulated in a tissue-specific fashion that reveals the subdivision of the mesoderm before its derivatives are overtly differentiated; e.g., the appearance of the notochord, myotomes, and pronephroi are preceded by the disappearance of Xsna mRNA, while undifferentiated mesoderm remains labelled, even into tadpole stages. Xsna is expressed in the suprablastoporal endoderm during gastrulation and in its derivatives, the prechordal and sub-notochordal endoderm, during neurulation. Relationships between Xbra, Xtwi, and Xsna expression are examined.Xsna is also expressed in the prospective neural fold ectoderm from stage 11 in a low arc above the dorsal marginal zone, precisely identifying a distinct band of cells that surrounds the prospective neural plate that we designate the neural plate border. The anterior transverse neural fold, which becomes forebrain, ceases Xsna expression during neurulation. In the longitudinal neural folds, the deep and superficial ectoderm compartments labelled by Xsna expression are the prospective neural crest and prospective roof of the neural tube, respectively. Xsna expression persists in the neural crest during migration and in some derivatives at least until metamorphosis but ceases in the roof of the neural tube soon after neurulation. 0 1993 Wiley-Liss, Inc.

Identification of neural crest competence territory: Role of Wnt signaling

“…Finally, we should mention that many recent experiments show the role of a number of transcription factors in neural crest induction (for a review, see Mayor and Aybar, 2001;, including Snail Essex et al, 1993;Linker et al, 2000;Aybar et al, 2003), Slug (Mayor et al, 1995), Zic5 (Nakata et al, 2000), FoxD3 (Dirksen and Jamrich, 1995;Sasai et al, 2001), Twist (Hopwood et al, 1989), Sox9 (Spokony et al, 2002), and Sox10 (Aoki et al, 2003;Honoré et al, 2003). The overexpression of these factors leads to an expansion of neural crest exactly in the region that we have identified as the neural crest competence territory.…”

The Proto-oncogene Transcription Factor Ets1 Regulates Neural Crest Development through Histone Deacetylase 1 to Mediate Output of Bone Morphogenetic Protein Signaling

“…These signaling pathways orchestrate and firstly activate neural plate border (NPB) specifiers including Pax3, Msx1 (7), and Zic1 (8), which establish a broad competence domain at the NPB. The cooperation of NPB specifiers, especially Pax3 and Zic1 (8,9), induces more restrictedly localized NC specifiers including c-Myc (10), Foxd3 (11,12), Sox9 (13), Snail1 (14,15), Snail2 (16), Tfap2 (17), and Id3 (18,19), which coordinate each other to regulate NC delamination and migration. The gene regulatory network of NC formation is conserved across vertebrate including zebrafish, frog, and mouse (20).…”

The mother superior mutation ablates foxd3 activity in neural crest progenitor cells and depletes neural crest derivatives in zebrafish

“…The development of NC progenitors is regulated by a well-orchestrated network of transcription factors that control specification, migration, and differentiation processes (Knecht and Bronner-Fraser, 2002). A number of such modulators have been identified including the zinc finger transcriptional repressors Slug and Snail and their related orthologues (Nieto et al, 1994;Essex et al, 1993;Thisse et al, 1995;Locascio et al, 2002;Barrallo-Gimeno and Nieto, 2005); the HMG Box-containing genes Sox8 (Bell et al, 2000), Sox9 (Chiang et al, 2001;Briscoe, 2003, Yan et al, 2002), and Sox10 (Southard-Smith et al, 1998;Dutton et al, 2001); the AP-2 family member tfap2a (BarralloGimeno et al, 2004;Knight et al, 2003;Mitchell et al, 1991); and the forkhead-box containing transcription factor FoxD3 (Dottori et al, 2001;Kos et al, 2001;Labosky and Kaestner, 1998;Odenthal and Nusslein-Volhard 1998). Mutations in these genes affect distinct stages of NC development, or differentiation of specific NC derivatives (reviewed by Huang and SaintJeannet, 2004;Gammill and BronnerFraser, 2003).…”