The Ste20 kinase misshapen is essential for the invasive behaviour of ovarian epithelial cells in Drosophila

Stationary‐to‐migratory transitions of epithelial cells have a key role in development and tumour progression. Border cell migration is a powerful system in which to investigate this transition in living organisms. Here, we identify the Ste20‐like kinase misshapen ( msn ) as a novel regulator of bor...

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Bibliographic Details
Published in:EMBO reports 2010-12, Vol.11 (12), p.943-949
Main Authors: Cobreros-Reguera, Laura, Fernández-Miñán, Ana, Fernández-Espartero, Cecilia H, López-Schier, Hernán, González-Reyes, Acaimo, Martín-Bermudo, María D
Format: Article
Language:English
Subjects:
Animals
Cadherins - genetics
CCAAT-Enhancer-Binding Proteins - metabolism
Cell adhesion & migration
cell migration
Cell Movement
DE-cadherin
Drosophila melanogaster - cytology
Drosophila melanogaster - enzymology
Drosophila Proteins - metabolism
EMBO05
EMBO11
Epithelial Cells - cytology
Epithelial Cells - enzymology
Female
Insects
JNK Mitogen-Activated Protein Kinases - metabolism
Kinases
Molecular biology
Ovary - cytology
Protein-Serine-Threonine Kinases - metabolism
Proteins
rab GTP-Binding Proteins - metabolism
Scientific Report
Scientific Reports
Signal Transduction
signalling
Ste20 kinases
Transcription, Genetic
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Summary:Stationary‐to‐migratory transitions of epithelial cells have a key role in development and tumour progression. Border cell migration is a powerful system in which to investigate this transition in living organisms. Here, we identify the Ste20‐like kinase misshapen ( msn ) as a novel regulator of border‐cell migration in Drosophila . Expression of msn in border cells is independent of the transcription factor slow border cells and of inputs from all pathways that are known to control border‐cell migration. The msn gene functions to modulate the levels and/or distribution of Drosophila E‐cadherin to promote the invasive migratory behaviour of border cells. This study identifies the Ste‐20‐like kinase misshapen as a key, novel regulator of the levels and/or distribution of DE‐Cadherin during collective cell migration.
ISSN:1469-221X
1469-3178
DOI:10.1038/embor.2010.156