Document Detail


Inhibition of patterned cell shape change and cell invasion by Discs large during Drosophila oogenesis.
MedLine Citation:
PMID:  9334318     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Drosophila Discs large (Dlg) is a tumor suppressor gene whose loss in epithelial tissues causes disrupted cell polarity and increased cell proliferation. A human Dlg homolog, hDlg, has been implicated in tumorigenic processes via its association with the product of the Adenomatous Polyposis Coli (APC) gene. We show for the first time that Drosophila Dlg is required to block cell invasion. Loss of dlg activity during oogenesis causes follicle cells to change shape and invade in a pattern similar to border cells, a small population of cells that break from the post-mitotic follicular epithelium during wild-type oogenesis, yet dlg mutant cells have not adopted a border cell fate. Both functional and morphological evidence indicates that cooperation between germ cell and follicle cell Dlg, probably mediated by Dlg PDZ domains, is crucial for regulating cell mixing, suggesting a novel developmental mechanism and mode of action for the Dlg family of molecules. These findings suggest that Dlg does not simply inhibit individual cell behaviors during oogenesis, but rather acts in a developmental pathway essential for blocking cell proliferation and migration in a spatio-temporally defined manner. A model for Dlg action in blocking cell invasion is presented.
Authors:
S Goode; N Perrimon
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Genes & development     Volume:  11     ISSN:  0890-9369     ISO Abbreviation:  Genes Dev.     Publication Date:  1997 Oct 
Date Detail:
Created Date:  1997-11-06     Completed Date:  1997-11-06     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  8711660     Medline TA:  Genes Dev     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2532-44     Citation Subset:  IM    
Affiliation:
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. goode@rascal.med.harvard.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Movement
Cell Size / genetics*
Clone Cells
Drosophila / cytology,  genetics,  physiology*
Drosophila Proteins*
Female
Genes, Insect*
Genes, Reporter / genetics
Genes, Tumor Suppressor*
Insect Proteins / genetics*,  physiology
Membrane Proteins / genetics,  metabolism
Microscopy, Confocal
Mutation
Nerve Tissue Proteins / genetics,  metabolism
Oocytes / cytology,  growth & development
Oogenesis*
Ovary / chemistry,  cytology,  growth & development
Phenotype
Protein Tyrosine Phosphatases*
Tumor Suppressor Proteins*
Grant Support
ID/Acronym/Agency:
GM17511-02/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Drosophila Proteins; 0/Insect Proteins; 0/Membrane Proteins; 0/Nerve Tissue Proteins; 0/Tumor Suppressor Proteins; 143513-41-1/discs large 1 protein, Drosophila; EC 3.1.3.48/Kek1 protein, Drosophila; EC 3.1.3.48/Protein Tyrosine Phosphatases
Comments/Corrections

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


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