PUBLICATION

Fgf, Hh, and pax2a differentially regulate expression of pax5 and pou3f3b in vestibular and auditory maculae in the zebrafish otic vesicle

Authors
Tan, A.L., Christensen, S.E., Baker, A.K., Riley, B.B.
ID
ZDB-PUB-230513-37
Date
2023
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   252(10): 1269-1279 (Journal)
Registered Authors
Riley, Bruce
Keywords
atoh1a, atoh1b, hearing and balance, saccular macula, utricular macula
MeSH Terms
  • Animals
  • Ear, Inner*/metabolism
  • Fibroblast Growth Factor 1
  • Fibroblast Growth Factors
  • Hearing
  • Hedgehog Proteins
  • Mice
  • PAX2 Transcription Factor/genetics
  • PAX2 Transcription Factor/metabolism
  • Zebrafish*/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
37171017 Full text @ Dev. Dyn.
Abstract
The vertebrate inner ear contains distinct sensory epithelia specialized for auditory or vestibular function. In zebrafish, the first sensory epithelia form at opposite ends of the otic vesicle and are functionally distinct: the anterior utricular macula is essential for vestibular function whereas the posterior saccular macula is critical for hearing. Mechanisms distinguishing these maculae are not clear. Here, we examined the effects of manipulating Fgf or Hh on expression of pax5 and pou3f3b, unique markers of utricular and saccular identity. We also examined the roles of pax2a and atoh1a/b, early regulators of sensory specification.
fgf3 and fgf8a were uniquely required for pax5 and pou3f3b, respectively. Elevating Fgf or blocking Hh expanded expression of pax5 but repressed pou3f3b, while blocking Fgf had the opposite effect. Blocking sensory specification did not affect pax5 or pou3f3b, but both markers were lost in pax2a-/- mutants. Maintenance of pax2a expression requires Fgf, Hh and Pax2a itself.
Specification of utricular identity requires high Fgf and is repressed by Hh, whereas saccular identity requires Hh plus low Fgf. pax2a acts downstream of Fgf and Hh to maintain both fates. Comparison with mouse suggests this may reflect a broadly conserved developmental mechanism.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
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Mapping