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The Journal of Cell Biology
Article
License: CC BY NC SA
Data sources: UnpayWall
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PubMed Central
Other literature type . 2010
Data sources: PubMed Central
The Journal of Cell Biology
Article . 2010 . Peer-reviewed
Data sources: Crossref
UNC Dataverse
Article . 2010
Data sources: Datacite
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Rho1 regulates apoptosis via activation of the JNK signaling pathway at the plasma membrane

Authors: Neisch, Amanda L.; Speck, Olga; Stronach, Beth; Fehon, Richard G.;

Rho1 regulates apoptosis via activation of the JNK signaling pathway at the plasma membrane

Abstract

Precisely controlled growth and morphogenesis of developing epithelial tissues require coordination of multiple factors, including proliferation, adhesion, cell shape, and apoptosis. RhoA, a small GTPase, is known to control epithelial morphogenesis and integrity through its ability to regulate the cytoskeleton. In this study, we examine a less well-characterized RhoA function in cell survival. We demonstrate that the Drosophila melanogaster RhoA, Rho1, promotes apoptosis independently of Rho kinase through its effects on c-Jun NH2-terminal kinase (JNK) signaling. In addition, Rho1 forms a complex with Slipper (Slpr), an upstream activator of the JNK pathway. Loss of Moesin (Moe), an upstream regulator of Rho1 activity, results in increased levels of Rho1 at the plasma membrane and cortical accumulation of Slpr. Together, these results suggest that Rho1 functions at the cell cortex to regulate JNK activity and implicate Rho1 and Moe in epithelial cell survival.

Keywords

rho GTP-Binding Proteins, Cell Membrane, JNK Mitogen-Activated Protein Kinases, Membrane Proteins, Apoptosis, Epithelial Cells, MAP Kinase Kinase Kinases, Animals, Genetically Modified, Enzyme Activation, Drosophila melanogaster, Animals, Drosophila Proteins, Wings, Animal, RNA Interference, Research Articles, Signal Transduction

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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    70
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
70
Top 10%
Top 10%
Top 10%
Green
hybrid