Calcium is the switch in the moonlighting dual function of the ligand-activated receptor kinase phytosulfokine receptor 1

Cell Communication and Signaling

Short Report

Oziniel Ruzvidzo¹  Chris Gehring²  Lubna Freihat³  Helen R Irving³  David T Manallack³  Janet I Wheeler³  Victor Muleya³ 

[1]Department of Biological Sciences, North-West University, Private Bag X2046, 2735, Mmabatho, South Africa

[2]Division of Biological and Environmental Sciences and Engineering, 4700 King Abdullah University of Science and Technology, 23955-6900, Thuwal, Kingdom of Saudi Arabia

[3]Monash Institute of Pharmaceutical Sciences, Monash University, 381 Royal Parade, 3052, Parkville, VIC, Australia

关键词: Calcium;    Guanylate cyclase;    Kinase;    PSKR1;   

DOI  :  10.1186/s12964-014-0060-z

 received in 2014-06-04, accepted in 2014-09-11,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundA number of receptor kinases contain guanylate cyclase (GC) catalytic centres encapsulated in the cytosolic kinase domain. A prototypical example is the phytosulfokine receptor 1 (PSKR1) that is involved in regulating growth responses in plants. PSKR1 contains both kinase and GC activities however the underlying mechanisms regulating the dual functions have remained elusive.FindingsHere, we confirm the dual activity of the cytoplasmic domain of the PSKR1 receptor. We show that mutations within the guanylate cyclase centre modulate the GC activity while not affecting the kinase catalytic activity. Using physiologically relevant Ca2+ levels, we demonstrate that its GC activity is enhanced over two-fold by Ca2+ in a concentration-dependent manner. Conversely, increasing Ca2+ levels inhibits kinase activity up to 500-fold at 100 nM Ca2+.ConclusionsChanges in calcium at physiological levels can regulate the kinase and GC activities of PSKR1. We therefore propose a functional model of how calcium acts as a bimodal switch between kinase and GC activity in PSKR1 that could be relevant to other members of this novel class of ligand-activated receptor kinases.

【 授权许可】

Unknown   
© Muleya et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.