title: Possible involvement of MAP kinase pathways in acquired metal-tolerance induced by heat in plants.
abstract: Cross tolerance is a phenomenon that occurs when a plant, in resisting one form of stress, develops a tolerance to another form. Pretreatment with nonlethal heat shock has been known to protect cells from metal stress. In this study, we found that the treatment of rice roots with more than 25 muM of Cu(2+) caused cell death. However, heat shock pretreatment attenuated Cu(2+)-induced cell death. The mechanisms of the cross tolerance phenomenon between heat shock and Cu(2+) stress were investigated by pretreated rice roots with the protein synthesis inhibitor cycloheximide (CHX). CHX effectively block heat shock protection, suggesting that protection of Cu(2+)-induced cell death by heat shock was dependent on de novo protein synthesis. In addition, heat pretreatment downregulated ROS production and mitogen-activated protein kinase (MAPK) activities, both of which can be greatly elicited by Cu(2+) stress in rice roots. Moreover, the addition of purified recombinant GST-OsHSP70 fusion proteins inhibited Cu(2+)-enhanced MAPK activities in an in vitro kinase assay. Furthermore, loss of heat shock protection was observed in Arabidopsis mkk2 and mpk6 but not in mpk3 mutants under Cu(2+) stress. Taken together, these results suggest that the interaction of OsHSP70 with MAPKs may contribute to the cellular protection in rice roots from excessive Cu(2+) toxicity.
authors.affiliation: Department of Life Sciences, National Cheng Kung University, Tainan, 701, Taiwan.
authors.forename: Po-Yu
authors.initials: PY
authors.lastname: Chen
authors.forename: Kuo-Ting
authors.initials: KT
authors.lastname: Lee
authors.forename: Wen-Chang
authors.initials: WC
authors.lastname: Chi
authors.forename: Heribert
authors.initials: H
authors.lastname: Hirt
authors.forename: Ching-Chun
authors.initials: CC
authors.lastname: Chang
authors.forename: Hao-Jen
authors.initials: HJ
authors.lastname: Huang
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects*; D017360:Arabidopsis / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D029681:Arabidopsis Proteins / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D003300:Copper / Q000633:toxicity; D015536:Down-Regulation / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D018869:Heat-Shock Response / Q000187:drug effects; D006358:Hot Temperature; D008670:Metals / Q000633:toxicity*; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D012275:Oryza / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology*; D010766:Phosphorylation / Q000187:drug effects; D010940:Plant Proteins / Q000378:metabolism; D018517:Plant Roots / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D029681:Arabidopsis Proteins; D018840:HSP70 Heat-Shock Proteins; D008670:Metals; D010940:Plant Proteins; D017382:Reactive Oxygen Species; D003300:Copper; D048049:Extracellular Signal-Regulated MAP Kinases; C436293:MPK6 protein, Arabidopsis; D020928:Mitogen-Activated Protein Kinases; C488959:MKK2 protein, Arabidopsis; D020929:Mitogen-Activated Protein Kinase Kinases