..., loss of RA signaling does not affect foxi1 expression or otic competence, but instead results in delayed onset of fgf3 expression and impaired otic induction. fgf8 mutants depleted of RA signaling produce few otic cells, and these cells fail to form a vesicle, indicating that Fgf8 is the primary factor...

... that zebrafish embryos mutant for fgf3 and fgf8 do not express early EB placode markers, including foxi1 and pax2a . Mosaic analysis demonstrates that placodal cells must directly receive Fgf signals during a specific crucial period of development. Transplantation experiments and mutant analysis reveal...

... epibranchial placodes. Mosaic analyses confirm that endoderm is the source of the neurogenic signal. Using a morpholino knockdown approach, we find that fgf3 is required for the majority of placode cells to undergo neurogenesis. Tissue transplants demonstrate that fgf3 activity is specifically required...

...Justin Gage Crump; Lisa Maves; Nathan D. Lawson; Brant M. Weinstein; Charles B. Kimmel Fibroblast growth factor (Fgf) proteins are important regulators of pharyngeal arch development. Analyses of Fgf8 function in chick and mouse and Fgf3 function in zebrafish have demonstrated a role for Fgfs...

...`jumpstart' of otic specification that is maintained by the Dlx3b-Pax2a pathway. * Author for correspondence (e-mail: [email protected] ) 9 7 2004 © 2004. 2004 dlx3b fgf3 fgf8 foxi1 Inner ear Morpholino Otic placode pax8 pax2a sox9a sox9b Zebrafish...

... the first molecular evidence whereby sensory organs direct the development of the associated non-sensory components, the semicircular canals, in vertebrate inner ears. The phenotypes induced by both RCAS -Fgf3 and RCAS -Fgf10 are complicated and appear to involve several developmental processes...

... of the adenohypophyseal anlage; and survival, proliferation and differential specification of adenohypophyseal progenitor cells. Here, we investigate the role of Fgf3 during pituitary development in the zebrafish, analyzing lia / fgf3 null mutants. We show that Fgf3 signaling from the ventral diencephalon is required...

... for the activation of Fgf3 expression and the maintenance of Fgf10 and Bmp4 expression in the otic vesicle. Furthermore, loss of Six1 function alters the expression pattern of Nkx5.1 and Gata3 , indicating that Six1 is required for regional specification of the otic vesicle. Finally, our data suggest...

... vhnf1 gives cellular competence to respond to Fgf signals in a caudal hindbrain-specific manner. * Author for correspondence (e-mail: [email protected] ) 1 5 2003 © 2003. 2003 Vhnf1 Fibroblast growth factor Fgf3 Fgf8 Zebrafish Hindbrain Valentino Krox20 Rhombomere Neural...

..., is aberrant in that it invades the otic placode territory. foo is expressed in pharyngeal pouch endoderm and is required for pouch expression of pax8 and proper patterning of other markers in the pouch such as nkx2.3 . In foo/foo embryos, we observed a failure to maintain fgf3 expression in the pouches...

... SU5402 treatment. FGFR1 signaling regulates Fgfr1, Fgf1, Fgf3 and Bmp7 expression and indirectly regulates Fgf7, Fgf10 and Bmp4 . Exogenous FGFs and BMPs added to glands in culture reveal distinct effects on gland morphology. Glands cultured with SU5402 were then rescued with exogenous BMP7, FGF7...

... in the zebrafish hindbrain. Time-lapse analyses of zebrafish hindbrain development show that r4 forms first and hindbrain neuronal differentiation occurs first in r4. Two signaling molecules, FGF3 and FGF8, which are both expressed early in r4, are together required for the development of rhombomeres adjacent...

... is required for the regionalisation within the telencephalon. Finally, antisense experiments with morpholino-modified oligonucleotides suggest that zebrafish fgf3 , which is also expressed in the ANB, co-operates with fgf8 in subpallial development. ‡Author for correspondence (e-mail: [email protected]...

... patterns of both fgf8 and fgf3 . Through gain- and loss-of-function experiments, we demonstrate that Fgf8 and Fgf3 act in vivo to induce the expression of Spry4, which in turn can inhibit activity of these growth factors. When overexpressed at low doses, Spry4 induces loss of cerebellum and reduction...