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 myelin basic protein (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, protein phosphatase, and H+-ATPase might function in the plant iron-triggered signaling pathway in rice roots.
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