Document Detail


The proneural gene ascl1a is required for endocrine differentiation and cell survival in the zebrafish adenohypophysis.
MedLine Citation:
PMID:  16481349     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Hans-Martin Pogoda; Sophia von der Hardt; Wiebke Herzog; Carina Kramer; Heinz Schwarz; Matthias Hammerschmidt
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-02-15
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  133     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-02-27     Completed Date:  2006-05-22     Revised Date:  2014-09-16    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  1079-89     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Basic Helix-Loop-Helix Transcription Factors / genetics,  metabolism*
Cell Differentiation
Cell Survival
Diencephalon / embryology,  metabolism
Endocrine System / cytology*,  embryology,  metabolism*
Fibroblast Growth Factor 3 / metabolism
Gene Expression Regulation, Developmental
Microscopy, Electron
Mutation / genetics
Pituitary Gland, Anterior / cytology,  embryology*,  metabolism*
Zebrafish / embryology*,  genetics,  metabolism*
Zebrafish Proteins / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
R01 GM063904/GM/NIGMS NIH HHS; R01 GM063904-01/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Basic Helix-Loop-Helix Transcription Factors; 0/Fibroblast Growth Factor 3; 0/Zebrafish Proteins; 0/achaete-scute complex-like 1a protein, zebrafish; 0/fgf3 protein, zebrafish

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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