PUBLICATION

Atoh1a expression must be restricted by Notch signaling for effective morphogenesis of the posterior lateral line primordium in zebrafish

Authors
Matsuda, M., and Chitnis, A.B.
ID
ZDB-PUB-101011-18
Date
2010
Source
Development (Cambridge, England)   137(20): 3477-3487 (Journal)
Registered Authors
Chitnis, Ajay
Keywords
mind bomb, Posterior lateral line, Neuromasts, Morphogenesis, Zebrafish, Cadherins, FGF signaling, Lateral inhibition
MeSH Terms
  • Animals
  • In Situ Hybridization
  • Immunohistochemistry
  • Fibroblast Growth Factor 10/metabolism
  • Gene Regulatory Networks/physiology*
  • Signal Transduction/physiology*
  • Cadherins/metabolism
  • Basic Helix-Loop-Helix Transcription Factors/metabolism*
  • Zebrafish/embryology*
  • Zebrafish Proteins/metabolism
  • Lateral Line System/embryology*
  • Lateral Line System/metabolism
  • Receptors, Notch/metabolism*
  • Morphogenesis/physiology*
(all 14)
PubMed
20876657 Full text @ Development
Abstract
The posterior lateral line primordium (pLLp) migrates caudally, depositing neuromasts to establish the posterior lateral line system in zebrafish. A Wnt-dependent FGF signaling center at the leading end of the pLLp initiates the formation of `proneuromasts' by facilitating the reorganization of cells into epithelial rosettes and by initiating atoh1a expression. Expression of atoh1a gives proneuromast cells the potential to become sensory hair cells, and lateral inhibition mediated by Delta-Notch signaling restricts atoh1a expression to a central cell. We show that as atoh1a expression becomes established in the central cell, it drives expression of fgf10 and of the Notch ligand deltaD, while it inhibits expression of fgfr1. As a source of Fgf10, the central cell activates the FGF pathway in neighboring cells, ensuring that they form stable epithelial rosettes. At the same time, DeltaD activates Notch in neighboring cells, inhibiting atoh1a expression and ensuring that they are specified as supporting cells. When Notch signaling fails, unregulated atoh1a expression reduces Fgfr1 expression, eventually resulting in attenuated FGF signaling, which prevents effective maturation of epithelial rosettes in the pLLp. In addition, atoh1a inhibits e-cadherin expression, which is likely to reduce cohesion and contribute to fragmentation of the pLLp. Together, our observations reveal a genetic regulatory network that explains why atoh1a expression must be restricted by Notch signaling for effective morphogenesis of the pLLp.
Genes / Markers
Figures
Figure Gallery (18 images) / 2
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Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b420
    		Point Mutation
    m132
      		Point Mutation
      m178
        		Point Mutation
        ta52b
          		Point Mutation
          zf106TgTransgenic Insertion
            1 - 5 of 5
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            Human Disease / Model
            No data available
            Sequence Targeting Reagents
            Target Reagent Reagent Type
            atoh1aMO1-atoh1aMRPHLNO
            atoh1bMO1-atoh1bMRPHLNO
            notch1aMO1-notch1aMRPHLNO
            notch3MO1-notch3MRPHLNO
            tp53MO4-tp53MRPHLNO
            1 - 5 of 5
            Show
            Fish
            Fish
            mib1m132/m132
            mib1m178/m178
            mib1ta52b/ta52b
            notch1ab420
            zf106Tg
            1 - 5 of 5
            Show
            Antibodies
            Orthology
            No data available
            Engineered Foreign Genes
            Marker Marker Type Name
            EGFPEFGEGFP
            1 - 1 of 1
            Show
            Mapping
            No data available
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            Citation
            Matsuda, M., and Chitnis, A.B. (2010) Atoh1a expression must be restricted by Notch signaling for effective morphogenesis of the posterior lateral line primordium in zebrafish. Development (Cambridge, England). 137(20):3477-3487.