Document Detail


Repression of Wasp by JAK/STAT signalling inhibits medial actomyosin network assembly and apical cell constriction in intercalating epithelial cells.
MedLine Citation:
PMID:  19934015     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Tissue morphogenesis requires stereotyped cell shape changes, such as apical cell constriction in the mesoderm and cell intercalation in the ventrolateral ectoderm of Drosophila. Both processes require force generation by an actomyosin network. The subcellular localization of Myosin-II (Myo-II) dictates these different morphogenetic processes. In the intercalating ectoderm Myo-II is mostly cortical, but in the mesoderm Myo-II is concentrated in a medial meshwork. We report that apical constriction is repressed by JAK/STAT signalling in the lateral ectoderm independently of Twist. Inactivation of the JAK/STAT pathway causes germband extension defects because of apical constriction ventrolaterally. This is associated with ectopic recruitment of Myo-II in a medial web, which causes apical cell constriction as shown by laser nanosurgery. Reducing Myo-II levels rescues the JAK/STAT mutant phenotype, whereas overexpression of the Myo-II heavy chain (also known as Zipper), or constitutive activation of its regulatory light chain, does not cause medial accumulation of Myo-II nor apical constriction. Thus, JAK/STAT controls Myo-II localization by additional mechanisms. We show that regulation of actin polymerization by Wasp, but not by Dia, is important in this process. Constitutive activation of Wasp, a branched actin regulator, causes apical cell constriction and promotes medial 'web' formation. Wasp is inactivated at the cell cortex in the germband by JAK/STAT signalling. Lastly, wasp mutants rescue the normal cortical enrichment of Myo-II and inhibit apical constriction in JAK/STAT mutants, indicating that Wasp is an effector of JAK/STAT signalling in the germband. We discuss possible models for the role of Wasp activity in the regulation of Myo-II distribution.
Authors:
Claire Bertet; Matteo Rauzi; Thomas Lecuit
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  136     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2010-02-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  4199-212     Citation Subset:  IM    
Affiliation:
IBDML, UMR6216 CNRS-Universit? de la M?diterran?e, Campus de Luminy, case 907, 13288 Marseille Cedex 09, France.
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MeSH Terms
Descriptor/Qualifier:
Actomyosin / metabolism
Animals
Cell Polarity / physiology
Cytoskeleton / metabolism
Drosophila / embryology,  physiology*
Drosophila Proteins / antagonists & inhibitors,  physiology*
Ectoderm / embryology,  physiology
Epithelial Cells* / cytology,  physiology
Janus Kinases / physiology
Mesoderm / embryology,  physiology
Morphogenesis / physiology
Myosin Type II / physiology
STAT Transcription Factors / physiology
Signal Transduction*
Wiskott-Aldrich Syndrome Protein / antagonists & inhibitors,  physiology*
Chemical
Reg. No./Substance:
0/Drosophila Proteins; 0/STAT Transcription Factors; 0/WASp protein, Drosophila; 0/Wiskott-Aldrich Syndrome Protein; 9013-26-7/Actomyosin; EC 2.7.10.2/Janus Kinases; EC 3.6.1.-/Myosin Type II

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