Early events in the signal pathway for the activation of MAPKs in rice roots exposed to iron

• Main Authors: Tsung-Mu Tsai, 蔡宗穆
• Other Authors: Hao-Jen Huang
• Format: Others
• Language: en_US
• Published: 2006
• Online Access: http://ndltd.ncl.edu.tw/handle/96491228639240198494

碩士 === 國立成功大學 === 生命科學系碩博士班 === 94 === 　Iron is an essential micronutrient for normal growth and development of plants. However, at high concentrations iron can become toxic to plants. Very little information is known about the molecular mechanism responsible for the regulation of plant growth by excess iron. The aim of this study was to investigate the signal transduction pathway activated by increasing concentrations (0.5, 1.0, and 2.5 mM) of iron. We showed that iron elicited a remarkable MBP kinase activity. By western blot and immunoprecipitation analysis, we suggested that iron-activated 42-kDa MBP kinase is a mitogen-activated protein kinase (MAPK). Cell death in rice roots due to iron toxicity was investigated using inhibitors of signal molecules known to regulate programmed cell death in plants. Phenylarsine oxide (PAO) and sodium orthovanadate, known inhibitors of tyrosine phosphatase, reduced iron-induced root cell death, but, cantharidin and endothall two-serine/threonine phosphatase inhibitor enhanced iron-induced root cell death. Moreover, our results revealed that H+-ATPase might participate in iron-induced cell death. These results suggested that the MAPK, reactive oxygen species (ROS), potassium channel, protein phosphatase, and H+-ATPase might function in the plant iron-triggered signalling pathway in rice roots. With analysis of the rice genome database, we identified eleven dual specificity phosphotases in rice genome. We found some dual-specificity phosphatases of gene expression pattern could be induced by vanadate. The pyronitrophenyl phosphatase (pNPP) was used as substrate and the phosphatase activity of OsDSP11 were measured in the present study.