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doi: 10.1242/10.1242/dev.00502
1 Department of Biopharmaceutical Sciences, Programs in Human Genetics,
Developmental Biology, Genetics, and Neuroscience, University of California,
San Francisco, CA 94143-0446, USA
2 Laboratory of Molecular Biophysics, The Rockefeller University, New York, NY
10021-6399,USA
* Author for correspondence (e-mail: suguo{at}itsa.ucsf.edu)
Accepted 20 March 2003
Vertebrate epibranchial placodes give rise to visceral sensory neurons that transmit vital information such as heart rate, blood pressure and visceral distension. Despite the pivotal roles they play, the molecular program underlying their development is not well understood. Here we report that the zebrafish mutation no soul, in which epibranchial placodes are defective, disrupts the fork headrelated, winged helix domain-containing protein Foxi1. Foxi1 is expressed in lateral placodal progenitor cells. In the absence of foxi1 activity, progenitor cells fail to express the basic helix-loop-helix gene neurogenin that is essential for the formation of neuronal precursors, and the paired homeodomain containing gene phox2a that is essential for neuronal differentiation and maintenance. Consequently, increased cell death is detected indicating that the placodal progenitor cells take on an apoptotic pathway. Furthermore, ectopic expression of foxi1 is sufficient to induce phox2a-positive and neurogenin-positive cells. Taken together, these findings suggest that Foxi1 is an important determination factor for epibranchial placodal progenitor cells to acquire both neuronal fate and subtype visceral sensory identity.
Key words: epibranchial placodes, foxi1, phox2a, Neurogenin, Zebrafish, Visceral sensory neurons
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