Casein Kinase Iγ2 Impairs Fibroblasts Actin Stress Fibers Formation and Delays Cell Cycle Progression in G1. (7th March 2012)

• Record Type: Journal Article
• Authors: Latreille, Mathieu; Abu-Thuraia, Afnan; Oliva, Rossella; Zuo, Dongmei; Larose, Louise
• Other Names: Pon Liza Academic Editor.
• Is Part Of: International journal of cell biology. Volume 2012(2012)
• Publication Date: 2012-03-07
• Subjects: Cytology -- Periodicals; Cell Biology; Cytology; Periodicals; Electronic journals -- Sciences; Electronic journals -- Biology; Periodicals; 571.6
• DOI: 10.1155/2012/684684
• Languages: English
• ISSNs: 1687-8876

Abstract

Abstract : Actin cytoskeleton remodeling is under the regulation of multiple proteins with various activities. Here, we demonstrate that the γ 2 isoform of Casein Kinase I (CKI γ 2) is part of a novel molecular path regulating the formation of actin stress fibers. We show that overexpression of CKI γ 2 in fibroblasts alters cell morphology by impairing actin stress fibers formation. We demonstrate that this is concomitant with increased phosphorylation of the CDK inhibitor p 27 Kip and lower levels of activated RhoA, and is dependent on CKI γ 2 catalytic activity. Moreover, we report that roscovitine, a potent inhibitor of cyclin-dependent kinases, including Cdk5, decreases p 27 Kip protein levels and restores actin stress fibers formation in CKI γ 2 overexpressing cells, suggesting the existence of a CKI γ 2-Cdk5-p 27 Kip -RhoA pathway in regulating actin remodeling. On the other hand, we also show that in a manner independent of its catalytic activity, CKI γ 2 delays cell cycle progression through G1. Collectively our findings reveal that CKI γ 2 is a novel player in the control of actin cytoskeleton dynamics and cell proliferation.