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Mesodermal Fgf10b cooperates with other fibroblast growth factors during induction of otic and epibranchial placodes in zebrafish
Author(s) -
Maulding Kirstin,
Padanad Mahesh S.,
Dong Jennifer,
Riley Bruce B.
Publication year - 2014
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.24119
Subject(s) - biology , zebrafish , otic vesicle , fgf8 , microbiology and biotechnology , fibroblast growth factor , mesoderm , embryonic induction , fgf10 , anatomy , genetics , embryonic stem cell , in situ hybridization , gene , gene expression , receptor
Background : Vertebrate otic and epibranchial placodes develop in close proximity in response to localized fibroblast growth factor (Fgf) signaling. Although less is known about epibranchial induction, the process of otic induction in highly conserved, with important roles for Fgf3 and Fgf8 reported in all species examined. Fgf10 is also critical for otic induction in mouse, but the only zebrafish ortholog examined to date, fgf10a , is not expressed early enough to play such a role. A second zebrafish ortholog, fgf10b , has not been previously examined. Results: We find that zebrafish fgf10b is expressed at tailbud stage in paraxial cephalic mesoderm beneath prospective epibranchial tissue, lateral to the developing otic placode. Knockdown of fgf10b does not affect initial otic induction but impairs subsequent accumulation of otic cells. Formation of epibranchial placodes and ganglia are also moderately impaired. Combinatorial disruption of fgf10b and fgf3 exacerbates the deficiency of otic cells and eliminates epibranchial induction entirely. Disruption of fgf10b and fgf24 also strongly reduces, but does not eliminate, epibranchial induction. Conclusions: fgf10b participates in a late phase of otic induction and, in combination with fgf3 , is especially critical for epibranchial induction. Developmental Dynamics 243:1275–1285, 2014 . © 2014 Wiley Periodicals, Inc.