Document Detail


Torso RTK controls Capicua degradation by changing its subcellular localization.
MedLine Citation:
PMID:  23048183     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The transcriptional repressor Capicua (Cic) controls multiple aspects of Drosophila embryogenesis and has been implicated in vertebrate development and human diseases. Receptor tyrosine kinases (RTKs) can antagonize Cic-dependent gene repression, but the mechanisms responsible for this effect are not fully understood. Based on genetic and imaging studies in the early Drosophila embryo, we found that Torso RTK signaling can increase the rate of Cic degradation by changing its subcellular localization. We propose that Cic is degraded predominantly in the cytoplasm and show that Torso reduces the stability of Cic by controlling the rates of its nucleocytoplasmic transport. This model accounts for the experimentally observed spatiotemporal dynamics of Cic in the early embryo and might explain RTK-dependent control of Cic in other developmental contexts.
Authors:
Oliver Grimm; Victoria Sanchez Zini; Yoosik Kim; Jordi Casanova; Stanislav Y Shvartsman; Eric Wieschaus
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  139     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-10     Completed Date:  2012-12-20     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  3962-8     Citation Subset:  IM    
Affiliation:
Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Body Patterning / genetics,  physiology
Drosophila
Drosophila Proteins / genetics,  metabolism*
Female
Fluorescence Recovery After Photobleaching
Gene Expression Regulation, Developmental / genetics,  physiology
HMGB Proteins / genetics,  metabolism*
Male
Receptor Protein-Tyrosine Kinases / genetics,  metabolism*
Repressor Proteins / genetics,  metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / genetics,  physiology
Grant Support
ID/Acronym/Agency:
P50-GM-071508/GM/NIGMS NIH HHS; R01 GM086537/GM/NIGMS NIH HHS; R01-GM077599/GM/NIGMS NIH HHS; R01GM086537/GM/NIGMS NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/Drosophila Proteins; 0/HMGB Proteins; 0/Repressor Proteins; 0/cic protein, Drosophila; EC 2.7.1.-/torso protein, Drosophila; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases
Comments/Corrections

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