Casein Kinase Iγ2 Impairs Fibroblasts Actin Stress Fibers Formation and Delays Cell Cycle Progression in G1. (28th December 2011)

• 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: 2011-12-28
• 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 inhibitorp 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, decreasesp 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.