PUBLICATION

The proneural gene ascl1a is required for endocrine differentiation and cell survival in the zebrafish adenohypophysis

Authors
Pogoda, H.M., von der Hardt, S., Herzog, W., Kramer, C., Schwarz, H., and Hammerschmidt, M.
ID
ZDB-PUB-060227-5
Date
2006
Source
Development (Cambridge, England)   133(6): 1079-1089 (Journal)
Registered Authors
Hammerschmidt, Matthias, Herzog, Wiebke, Pogoda, Hans-Martin, von der Hardt, Sophia
Keywords
Ascl1a (Zash1a), Pituitary, Adenohypophysis, Neurohypophysis, Zebrafish, Pia, Cell survival, Cell specification, Apoptosis
MeSH Terms
  • Animals, Genetically Modified
  • Cell Differentiation
  • Fibroblast Growth Factor 3/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Basic Helix-Loop-Helix Transcription Factors/metabolism*
  • Animals
  • Cell Survival
  • Pituitary Gland, Anterior/cytology
  • Pituitary Gland, Anterior/embryology*
  • Pituitary Gland, Anterior/metabolism*
  • Microscopy, Electron
  • Mutation/genetics
  • Gene Expression Regulation, Developmental
  • Endocrine System/cytology*
  • Endocrine System/embryology
  • Endocrine System/metabolism*
  • Diencephalon/embryology
  • Diencephalon/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
(all 23)
PubMed
16481349 Full text @ Development
Abstract
Mammalian basic helix-loop-helix proteins of the achaete-scute family are proneural factors that, in addition to the central nervous system, are required for the differentiation of peripheral neurons and sensory cells, derivatives of the neural crest and placodal ectoderm. Here, in identifying the molecular nature of the pia mutation, we investigate the role of the zebrafish achaete-scute homologue ascl1a during development of the adenohypophysis, an endocrine derivative of the placodal ectoderm. Similar to mutants deficient in Fgf3 signaling from the adjacent ventral diencepahalon, pia mutants display failure of endocrine differentiation of all adenohypophyseal cell types. Shortly after the failed first phase of cell differentiation, the adenohypophysis of pia mutants displays a transient phase of cell death, which affects most, but not all adenohypophyseal cells. Surviving cells form a smaller pituitary rudiment, lack expression of specific adenohypophyseal marker genes (pit1, neurod), while expressing others (lim3, pitx3), and display an ultrastructure reminiscent of precursor cells. During normal development, ascl1a is expressed in the adenohypophysis and the adjacent diencephalon, the source of Fgf3 signals. However, chimera analyses show that ascl1a is required cell-autonomously in adenohypophyseal cells themselves. In fgf3 mutants, adenohypophyseal expression of ascl1a is absent, while implantation of Fgf3-soaked beads into pia mutants enhances ascl1a, but fails to rescue pit1 expression. Together, this suggests that Ascl1a might act downstream of diencephalic Fgf3 signaling to mediate some of the effects of Fgf3 on the developing adenohypophysis.
Genes / Markers
Figures
Figure Gallery (6 images)
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Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
fgf3_unspecified
    Unspecified
    t25215
      Point Mutation
      1 - 2 of 2
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      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      ascl1aMO1-ascl1aMRPHLNO
      1 - 1 of 1
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      Fish
      Antibodies
      No data available
      Orthology
      No data available
      Engineered Foreign Genes
      No data available
      Mapping
      Entity Type Entity Symbol Location
      Featuret25215Chr: 18 Details
      SSLPz11566Chr: 4 Details
      SSLPz27201Chr: 4 Details
      1 - 3 of 3
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