The expression of a zebrafish gene homologous to Drosophila snail suggests a conserved function in invertebrate and vertebrate gastrulation
- Hammerschmidt, M. and Nüsslein-Volhard, C.
- Development (Cambridge, England) 119: 1107-1118 (Journal)
- Registered Authors
- Hammerschmidt, Matthias, Nüsslein-Volhard, Christiane
- MeSH Terms
- Amino Acid Sequence
- Base Sequence
- Blotting, Western
- Conserved Sequence*
- Gene Expression/physiology*
- Molecular Sequence Data
- Neural Crest/physiology
- 8306877 Full text @ Development
Hammerschmidt, M. and Nüsslein-Volhard, C. (1993) The expression of a zebrafish gene homologous to Drosophila snail suggests a conserved function in invertebrate and vertebrate gastrulation. Development (Cambridge, England). 119:1107-1118.
Snail, a zinc finger protein, is required for the formation of the ventral furrow and the mesoderm during gastrulation of the Drosophila embryo. snail homologues have been cloned from Xenopus and mouse. We have isolated a zebrafish homologue of snail, designated sna-1. Like its Drosophila counterpart, Sna-1 protein is nuclear. Maternal and zygotic sna-1 transcripts are ubiquitously distributed in zebrafish embryos of cleavage and blastula stages. In gastrulating embryos, sna-1 is expressed in involuting cells of the germ ring, but not in those at the dorsal midline, the presumptive notochordal region. After involution, the expression is maintained in the paraxial mesoderm and becomes prominent in the muscle pioneer precursors, followed by expression at the posterior somite boundaries. Later, sna-1 is expressed in neural crest and mesodermal derivatives of the head region. Sna-1 expression is induced in animal cap cells by activin A. The early sna-1 expression pattern in gastrulating zebrafish no tail (ntl) mutant embryos is normal except a reduction in the level of sna-1 transcription, suggesting that Ntl protein is not the key activator of sna-1 transcription in vivo, but might be involved in the enhancement or maintenance of sna-1 transcription. Data obtained in studies with ectopic ntl expression support this model.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes