THE VENTRAL AND POSTERIOR EXPRESSION OF THE ZEBRAFISH HOMEOBOX GENE EVE1 IS PERTURBED IN DORSALIZED AND MUTANT EMBRYOS
By J.-S. Joly1, C. Joly2, S. Schulte-Merker3, H. Boulekbache2, and H. Condamine1
1 Unité de Génétique des Mammifères, Institut Pasteur, 25 rue du Docteur Roux, F-75724 Paris Cedex 15, FRANCE; 2 Laboratoire de Biologie du Développement, Université Paris 7, 7 quai St-Bernard, F-75251 Paris Cedex 05, FRANCE; 3 Laboratory of Developmental Biology, NIMR, The Ridgeway, Mill Hill, London NW7 1AA, UNITED KINGDOM.
We have identified and characterized zebrafish eve1, a novel member of the Drosophila even-skipped (eve) gene family. eve1 RNAs are expressed initially in late blastulae with a peak during the gastrula stage, at which time expression is confined to ventral and lateral cells of the marginal zone of the zebrafish embryo. Later, eve1 transcripts are located in the most posterior part of the extending tail tip. We show that LiCl, known to dorsalize Xenopus embryos, has the same effect in zebrafish, resulting in embryos with exaggerated dorsoanterior structures. In LiCl-treated embryos, eve1 transcripts are completely absent. eve1 is therefore a marker of ventral and posterior mesoderm.
In the light of its ventroposterior expression domain, the localization of eve1 transcripts was analyzed in spadetail (spt) and no tail (ntl), two mutants with abnormal caudal development. In sptb140 homozygous mutants, there is an accumulation of cells in the tail region, resulting from inadequate migratory behavior of trunk somite cells. These cells, in their abnormal environment, express eve1, emphasizing the correlation between ventroposterior position and eve1 expression. In homozygous mutant embryos for the gene ntl (the homologue of mouse Brachyury, originally called Zf-T), posterior structures are missing (M.E. Halpern and C.B. Kimmel, personal communication). While mutant and wildtype embryos do not differ in their eve1 transcript distribution during gastrulation, eve1 expression is absent in the tail bud of mutant embryos during early somitogenesis, indicating a requirement for ntl in the maintenance of eve1 expression.
Our findings suggest that eve1 expression is correlated with a ventral and posterior cell fate, and provide first insights into its regulation.
Return to Contents