title: Involvement of abscisic acid-dependent and -independent pathways in the upregulation of antioxidant enzyme activity during NaCl stress in cotton callus tissue.
abstract: The role of abscisic acid (ABA) in the signal transduction pathway associated with NaCl-induced up-regulation of antioxidant enzyme activity was examined in a NaCl-tolerant cotton callus cell line treated with NaCl, ABA, paraquat, or H2O2 in the presence and absence or fluridone, an inhibitor of terpene, and therefore, ABA synthesis. Treatment with NaCl resulted in a rapid increase (within 30 minutes) in the ABA levels of the callus tissue, and the NaCl, ABA, and paraquat treatments induced rapid increases in the activities of superoxide dismutase, catalase, peroxidase, and glutathione reductase. Pre-treatment with fluridone significantly suppressed the NaCl-induced increases, but only slightly delayed the increases in tissue subjected to exogenous ABA treatment. This implies that ABA is involved in the signal transduction pathway associated with the NaCl-induced up-regulation of these antioxidant enzymes. Pre-treatment with fluridone had no effect on the paraquat-induced increases, suggesting that these enzymes can also be up-regulated by a pathway other than the one mediated by ABA. Both the NaCl and paraquat treatments produced significant increases in the superoxide levels within the callus, but the increase resulting from the paraquat treatment was significantly higher than the increase resulting from the NaCl treatment. These data suggest that NaCl stress results in the production of reactive oxygen intermediates (ROI) which signals the induction of an ABA-dependent signaling pathway. The production of very high levels of ROI, such as those that occur with paraquat treatment or perhaps during periods of prolonged or extreme stress, may induce an ABA-independent signaling pathway.
authors.affiliation: Department of Biological Sciences, Louisianna State University-Shreveport, 71115, USA.
authors.forename: B A
authors.initials: BA
authors.lastname: Bellaire
authors.forename: J
authors.initials: J
authors.lastname: Carmody
authors.forename: J
authors.initials: J
authors.lastname: Braud
authors.forename: D R
authors.initials: DR
authors.lastname: Gossett
authors.forename: S W
authors.initials: SW
authors.lastname: Banks
authors.forename: M C
authors.initials: MC
authors.lastname: Lucas
authors.forename: T E
authors.initials: TE
authors.lastname: Fowler
mesh_terms: D000040:Abscisic Acid / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000502:physiology*; D060387:Ascorbate Peroxidases; D002460:Cell Line; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005980:Glutathione Reductase / Q000378:metabolism; D003368:Gossypium / Q000166:cytology / Q000201:enzymology* / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000494:pharmacology; D018384:Oxidative Stress; D010088:Oxidoreductases / Q000037:antagonists & inhibitors; D010269:Paraquat / Q000494:pharmacology; D009195:Peroxidase / Q000378:metabolism; D010544:Peroxidases / Q000378:metabolism; D011728:Pyridones / Q000494:pharmacology; D015398:Signal Transduction; D012965:Sodium Chloride / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D004791:Enzyme Inhibitors; D011728:Pyridones; D013481:Superoxides; C013351:fluridone; D012965:Sodium Chloride; D000040:Abscisic Acid; D006861:Hydrogen Peroxide; D010088:Oxidoreductases; D010544:Peroxidases; D060387:Ascorbate Peroxidases; D009195:Peroxidase; C022398:phytoene dehydrogenase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D010269:Paraquat