The mechanism(s) of inhibitory effects of heavy metals on plant root growth and development

• Main Authors: Wan-Chi Hung, 洪琬琪
• Other Authors: Dinq-Ding Huang
• Format: Others
• Language: en_US
• Published: 2003
• Online Access: http://ndltd.ncl.edu.tw/handle/33650836556076964257

碩士 === 國立成功大學 === 生物學系碩博士班 === 91 === Heavy metal toxicity is one of the major environment health problems in modern society. Rapid industrialization and urbanization have enhanced the levels of toxic heavy metals in the environment posing a potential health hazard for all living organisms. In plants, these heavy metals when accumulated in excess amounts can function as stressors causing physiological constraints and alterations in various vital growth processes, such as transpiration, photosynthesis, enzyme activities. It has been known that heavy metals exert inhibitory effects in plant growth and development. However, the mechanism involved in its effect is not well understood. Roots of plants are damaged if the dose of heavy metals exceeds threshold levels. In this study, we used two model plants, Arabidopsis and rice, to study the molecular mechanism(s) of heavy metals on root growth and development. In Arabidopsis, the redifferentiation of adventitious roots from hypocotyl callus was severely damaged by Cd and Cu treatments. In rice, copper treatment caused the inhibition of root growth as well as the cell death and DNA fragmentation of root cells. Pre-treatment of rice roots with antioxidants (GSH, NAC, DTT), calcium chelator (EGTA), plasma-membrane calcium channel blocker (La3+), calmodulin antagonist (W-7), protein phosphatase inhibitors (sodium orthovanadate, cantharidin) and MAPK kinase (MEK) inhibitors (PD098059, U0126) blocked copper-induced cell death. We suggest that ROS production, extracellular calcium ions, protein phosphatase and activation of MAPK pathway are probably involved in copper-induced cell death of root-tip cells in rice. Protein phosphorylation and dephosphorylation are involved in the regulation of many eukaryotic intracellular processes. It has been known that heavy metals inhibit the proliferation and differentiation of cells in animals. The variations in protein tyrosine phosphorylation caused by heavy metals has been studied in mammalian cells. However, data related to the involvement of protein tyrosine phosphorylation in plant growth and development influenced by heavy metals was limited. In this study, the possible roles of protein tyrosine phosphorylation in cadmium-inhibited root development in Arabidopsis and copper-induced cell death of root-tip cells in rice were investigated. In cadmium- inhibited root development in Arabidopsis, a 80-kDa protein was highly tyrosine phosphorylated. In copper-induced cell death of rice root-tip cells, the level of tyrosine phosphorylation of a 45-kDa protein was decreased. Pre-treatment of rice roots with tyrosine phosphatase inhibitor sodium orthovanadate, the antioxidant GSH and the calcium chelator EGTA significantly abolished copper-induced protein tyrosine dephosphorylation. In addition, MAPKs play important roles in signal transduction in responses to biotic and abiotic stresses. Since OsMAPK2 function in specific stress-signalling pathway, the MAP kinase gene (OsMAPK2) expression in rice under copper stress was also investigated. OsMAPK2 transcript accumulation was enhanced by copper and H2O2 in rice root-tip cells. Using Northern blot analysis, it was shown that antioxidant agent (GSH), calcium chelator (EGTA), plasma-membrane calcium channel blocker (La3+) and protein phosphatase inhibitor (cantharidin) inhibited copper-induced OsMAPK2 gene expression. These results indicate that tyrosine phosphorylation/ dephosphorylation and activation of MAPK pathway are probably involved in heavy metals-inhibited root development in Arabidopsis and heavy metals-induced cell death of rice root-tip cells. These results provide some information for further studies on the mechanism(s) of heavy metal toxicity in plants.