Protection against heat stress-induced oxidative damage in Arabidopsis involves calcium, abscisic acid, ethylene, and salicylic acid.
Plants, in common with all organisms, have evolved mechanisms to cope with the problems caused by high temperatures. We examined specifically the involvement of calcium, abscisic acid (ABA), ethylene, and salicylic acid (SA) in the protection against heat-induced oxidative damage in Arabidopsis. Heat caused increased thiobarbituric acid reactive substance levels (an indicator of oxidative damage to membranes) and reduced survival. Both effects required light and were reduced in plants that had acquired thermotolerance through a mild heat pretreatment. Calcium channel blockers and calmodulin inhibitors increased these effects of heating and added calcium reversed them, implying that protection against heat-induced oxidative damage in Arabidopsis requires calcium and calmodulin. Similar to calcium, SA, 1-aminocyclopropane-1-carboxylic acid (a precursor to ethylene), and ABA added to plants protected them from heat-induced oxidative damage. In addition, the ethylene-insensitive mutant etr-1, the ABA-insensitive mutant abi-1, and a transgenic line expressing nahG (consequently inhibited in SA production) showed increased susceptibility to heat. These data suggest that protection against heat-induced oxidative damage in Arabidopsis also involves ethylene, ABA, and SA. Real time measurements of cytosolic calcium levels during heating in Arabidopsis detected no increases in response to heat per se, but showed transient elevations in response to recovery from heating. The magnitude of these calcium peaks was greater in thermotolerant plants, implying that these calcium signals might play a role in mediating the effects of acquired thermotolerance. Calcium channel blockers and calmodulin inhibitors added solely during the recovery phase suggest that this role for calcium is in protecting against oxidative damage specifically during/after recovery.
Larkindale
Jane
J
Department of Plant Sciences, University of Oxford, South Parks Road, Oxford OX1 3RB, United Kingdom. jane.larkindale@plants.ox.ac.uk
Knight
Marc R
MR
D000040:Abscisic Acid / Q000378:metabolism* / Q000494:pharmacology; D000598:Amino Acids, Cyclic / Q000378:metabolism / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000494:pharmacology; D002478:Cells, Cultured; D019610:Cytoprotection; D005030:Ethylenes / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006358:Hot Temperature; D008027:Light; D015227:Lipid Peroxidation / Q000187:drug effects; D009154:Mutation; D018384:Oxidative Stress / Q000187:drug effects; D030821:Plants, Genetically Modified; D020156:Salicylic Acid / Q000378:metabolism* / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000598:Amino Acids, Cyclic; D002121:Calcium Channel Blockers; D002147:Calmodulin; D005030:Ethylenes; D006360:Heat-Shock Proteins; D017392:Thiobarbituric Acid Reactive Substances; C023863:1-aminocyclopropane-1-carboxylic acid; D000040:Abscisic Acid; C036216:ethylene; D020156:Salicylic Acid; D002118:Calcium