title: Early signalling pathways in rice roots under vanadate stress.
abstract: Vanadate is beneficial to plant growth at low concentration. However, plant exposure to high concentrations of vanadate has been shown to arrest cell growth and lead to cell death. We are interested in understanding the signalling pathways of rice roots in response to vanadate stress. In this study, we demonstrated that vanadate induced rice root cell death and suppressed root growth. In addition, we found that vanadate induced ROS accumulation, increased lipid peroxidation and elicited a remarkable increase of MAPKs and CDPKs activities in rice roots. In contrast, pre-treatment of rice roots with ROS scavenger (sodium benzoate), serine/threonine protein phosphatase inhibitor (endothall), and CDPK antagonist (W7), reduced the vanadate-induced MAPKs activation. Furthermore, the expression of a MAPK gene (OsMPK3) and four tyrosine phosphatase genes (OsDSP3, OsDSP5, OsDSP6, and OsDSP10) were regulated by vanadate in rice roots. Collectively, these results strongly suggest that ROS, protein phosphatase, and CDPK may function in the vanadate-triggered MAPK signalling pathway cause cell death and retarded growth in rice roots.
authors.affiliation: Department of Life Sciences, National Cheng Kung University, Tainan, Taiwan.
authors.forename: Chung-Wen
authors.initials: CW
authors.lastname: Lin
authors.forename: Chung-Yi
authors.initials: CY
authors.lastname: Lin
authors.forename: Ching-Chun
authors.initials: CC
authors.lastname: Chang
authors.forename: Ruey-Hua
authors.initials: RH
authors.lastname: Lee
authors.forename: Tsung-Mu
authors.initials: TM
authors.lastname: Tsai
authors.forename: Po-Yu
authors.initials: PY
authors.lastname: Chen
authors.forename: Wen-Chang
authors.initials: WC
authors.lastname: Chi
authors.forename: Hao-Jen
authors.initials: HJ
authors.lastname: Huang
mesh_terms: D015153:Blotting, Western; D003998:Dicarboxylic Acids / Q000494:pharmacology; D004591:Electrophoresis, Polyacrylamide Gel; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D012275:Oryza / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D010940:Plant Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D018517:Plant Roots / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D011494:Protein Kinases / Q000378:metabolism; D054645:Protein Phosphatase 1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D036226:Seedlings / Q000235:genetics / Q000254:growth & development / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013449:Sulfonamides / Q000494:pharmacology; D013997:Time Factors; D014638:Vanadates / Q000494:pharmacology*; D017871:Calcium-Calmodulin-Dependent Protein Kinases
chemical_list: D003998:Dicarboxylic Acids; D004791:Enzyme Inhibitors; D008315:Malondialdehyde; D020928:Mitogen-Activated Protein Kinases; D010940:Plant Proteins; D011494:Protein Kinases; D054645:Protein Phosphatase 1; D017382:Reactive Oxygen Species; D013449:Sulfonamides; D014638:Vanadates; D017871:Calcium-Calmodulin-Dependent Protein Kinases; C100030:endothall; C017967:W 7