dictyNews
Electronic Edition
Volume 48, number 15
August 5, 2022

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Abstracts
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AKT and SGK Kinases Regulate Cell Migration by Altering Scar/WAVE 
Complex Activation and Arp2/3 Complex Recruitment.
 
Shashi Prakash Singh1,2*, Peggy Paschke1, Luke Tweedy1 and 
Robert H. Insall1,3,#.
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*Corresponding author: [log in to unmask]
 
Affiliations: 1CRUK Beatson Institute, Glasgow, UK, 2Research 
Institute of Infection, Immunity & Inflammation, University of 
Glasgow, UK, 3Institute of Cancer Sciences, University of Glasgow, 
Glasgow, UK.

 
Frontiers in Molecular Bioscience, in press

Cell polarity and cell migration both depend on pseudopodia and 
lamellipodia formation. These are regulated by coordinated 
signaling acting through G-protein coupled receptors and kinases 
such as PKB/AKT and SGK, as well as the actin cytoskeletal 
machinery. Here we show that both Dictyostelium PKB and SGK 
kinases (encoded by pkbA and pkgB) are dispensable for chemotaxis 
towards folate. However, both are involved in the regulation of 
pseudopod formation and thus cell motility. Cells lacking pkbA 
and pkgB showed a substantial drop in cell speed. Actin 
polymerization is perturbed in pkbA- and reduced in pkgB- and 
pkbA-/pkgB- mutants. The Scar/WAVE complex, key catalyst of 
pseudopod formation, is recruited normally to the fronts of all 
mutant cells (pkbA-, pkgB- and pkbA-/pkgB-), but is unexpectedly 
unable to recruit the Arp2/3 complex in cells lacking SGK.  
Consequently, loss of SGK causes a near-complete loss of normal 
actin pseudopodia, though this can be rescued by overexpression 
of PKB. Hence both PKB and SGK are required for correct assembly 
of F-actin and recruitment of the Arp2/3 complex by the Scar/WAVE 
complex during pseudopodia formation.


Submitted by Shashi Singh [[log in to unmask]]
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[End dictyNews, volume 48, number 15]