Document Detail


Jun mediates Frizzled-induced R3/R4 cell fate distinction and planar polarity determination in the Drosophila eye.
MedLine Citation:
PMID:  10903185     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Jun acts as a signal-regulated transcription factor in many cellular decisions, ranging from stress response to proliferation control and cell fate induction. Genetic interaction studies have suggested that Jun and JNK signaling are involved in Frizzled (Fz)-mediated planar polarity generation in the Drosophila eye. However, simple loss-of-function analysis of JNK signaling components did not show comparable planar polarity defects. To address the role of Jun and JNK in Fz signaling, we have used a combination of loss- and gain-of-function studies. Like Fz, Jun affects the bias between the R3/R4 photoreceptor pair that is critical for ommatidial polarity establishment. Detailed analysis of jun(-) clones reveals defects in R3 induction and planar polarity determination, whereas gain of Jun function induces the R3 fate and associated polarity phenotypes. We find also that affecting the levels of JNK signaling by either reduction or overexpression leads to planar polarity defects. Similarly, hypomorphic allelic combinations and overexpression of the negative JNK regulator Puckered causes planar polarity eye phenotypes, establishing that JNK acts in planar polarity signaling. The observation that Dl transcription in the early R3/R4 precursor cells is deregulated by Jun or Hep/JNKK activation, reminiscent of the effects seen with Fz overexpression, suggests that Jun is one of the transcription factors that mediates the effects of fz in planar polarity generation.
Authors:
U Weber; N Paricio; M Mlodzik
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  127     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-09-19     Completed Date:  2000-09-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  3619-29     Citation Subset:  IM    
Affiliation:
European Molecular Biology Laboratory, Developmental Biology Programme, Meyerhofstrasse 1, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Aspartic Acid
Cell Differentiation
Cell Polarity
Drosophila / embryology*
Drosophila Proteins*
Enzyme Activation
Eye / embryology*
Frizzled Receptors
Membrane Proteins / metabolism*
Mitogen-Activated Protein Kinase Kinases / metabolism*
Phenotype
Phosphoprotein Phosphatases / metabolism
Receptors, G-Protein-Coupled
Chemical
Reg. No./Substance:
0/Drosophila Proteins; 0/Frizzled Receptors; 0/Membrane Proteins; 0/Receptors, G-Protein-Coupled; 0/fz protein, Drosophila; 56-84-8/Aspartic Acid; EC 2.7.1.-/hemipterous protein, Drosophila; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases; EC 3.1.3.-/puc protein, Drosophila; EC 3.1.3.16/Phosphoprotein Phosphatases

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


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