dackel acts in the ectoderm of the zebrafish pectoral fin bud to maintain AER signaling

Classical embryological studies have implied the existence of an apical ect odermal maintenance factor (AEMF) that sustains signaling from the apical e ctodermal ridge (AER) during vertebrate limb development. Recent evidence s uggests that AEMF activity is composed of different signals involving both a sonic hedgehog (Shh) signal and a fibroblast growth factor 10 (Fgf10) sig nal from the mesenchyme. In this study we show that the product of the dack el (dak) gene is one of the components that acts in the epidermis of the ze brafish pectoral fin bud to maintain signaling from the apical fold, which is homologous to the AER of tetrapods, dak acts synergistically with Shh to induce fgf4 and fgf8 expression but independently of Shh in promoting apic al fold morphogenesis. The failure of dak mutant fin buds to progress from the initial fin induction phase to the autonomous outgrowth phase causes lo ss of both AER and Shh activity, and subsequently results in a proximodista l truncation of the fin, similar to the result obtained by ridge ablation e xperiments in the chicken. Further analysis of the dak mutant phenotype ind icates that the activity of the transcription factor engrailed 1 (En1) in t he ventral non-ridge ectoderm also depends on a maintenance signal probably provided by the ridge. This result uncovers a new interaction between the AER and the dorsoventral organizer in the zebrafish pectoral fin bud.