PKN-1, a homologue of mammalian PKN, is involved in the regulation of muscle contraction and force transmission in C. elegans

• Type of Material: Article
• Authors: Hiroshi Kadota, Emory University; Takayuki Miyauchi, Nara Institute of Science and Technology; John F. Nahabedian, Georgia Institute of Technology; Jeffrey N. Stirman, Georgia Institute of Technology; Hang Lu, Georgia Institute of Technology; Mutsuki Amano, Nara Institute of Science and Technology; Guy Benian, Emory University; Kozo Kaibuchi, Nara Institute of Science and Technology
• Language: English
• Date: 2011-03-25
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2011 Elsevier Ltd. All rights reserved.
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.1016/j.jmb.2011.01.039
• Title of Journal or Parent Work: Journal of Molecular Biology
• ISSN: 0022-2836
• Volume: 407
• Issue: 2
• Start Page: 222
• End Page: 231
• Grant/Funding Information: GMB was supported by NIAMS / NIH grant AR051466.; HL is supported by NIH (NIBIB-R21EB012803, NIA-R01AG035317), NSF (CBET/CAREER-0954578), and the Alfred P. Sloan Foundation.; The Genetics Center is funded by the National Institutes of Health (NIH) Center for Research Resources.; HQ, MA, and KK were supported by grants-in-aid for Scientific Research from the Ministry of Education, Science, and Culture, Japan, by the Japan Society of the Promotion of Science Research for the Future, by the Human Frontier Science Program.
• Keywords: PKN; Rho GTPase; muscle; contraction; C. elegans
• Research Categories: Biology, Molecular

Abstract

To examine the in vivo functions of protein kinase N (PKN), one of the effectors of Rho small GTPases, we used the nematode Caernorhabditis elegans as a genetic model system. We identified a C. elegans homologue (pkn-1) of mammalian PKN and confirmed direct binding to C. elegans Rho small GTPases. Using a GFP reporter, we showed that pkn-1 is mainly expressed in various muscles and is localized at dense bodies and M-lines. Over-expression of the PKN-1 kinase domain and loss-of-function mutations by genomic deletion of pkn-1 resulted in a loopy Unc phenotype, which has been reported in many mutants of neuronal genes. The results of mosaic analysis and body wall muscle specific expression of PKN-1 kinase domain suggests that this loopy phenotype is due to the expression of PKN-1 in body wall muscle. The genomic deletion of pkn-1 also showed a defect in force transmission. These results suggest that PKN-1 functions as a regulator of muscle contraction-relaxation and as a component of the force transmission mechanism.