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Early Pattering in the Zebrafish Inner Ear
Author(s) -
Riley Bruce B,
Padanad Mahesh
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.59.1
Subject(s) - zebrafish , fibroblast growth factor , microbiology and biotechnology , inner ear , biology , cell fate determination , otic vesicle , neuroscience , transcription factor , receptor , genetics , in situ hybridization , gene expression , gene
It is well established that Fgf signaling is essential for otic placode induction, but downstream mechanisms are still poorly characterized. In zebrafish, pax8 expression marks an early response to Fgf signaling. We show that pax8 mediates two key functions. First, it is necessary and sufficient to activate expression of fgf24 in newly specified otic cells. This appears to expand the otic field through ongoing recruitment. Second, pax8 cell‐autonomously represses foxi1, one of the co‐factors initially required to activate pax8. In addition to activation pax8, foxi1 plus Fgf also activate sox3, though in broader domain including both otic and epibranchial placodes. We find that failure to down‐regulate Foxi1 in prospective otic cells causes them to transfate to epibranchial fate. Thus, pax8 simultaneously maintains otic fate by blocking epibranchial fate and expands the otic territory by augmenting Fgf signaling. Supported by NIH‐NIDCD R01‐DC03806.