title: Calcium is involved in nitric oxide- and auxin-induced lateral root formation in rice.
abstract: In the present study, the role of nitric oxide (NO) in the regulation of lateral root (LR) formation in rice was examined. Application of sodium nitroprusside (SNP; a NO donor) and indole-3-butyric acid (IBA; a naturally occurring auxin) to rice seedlings induced LR formation. The effect is specific for NO because the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3- oxide (cPTIO) blocked the action of SNP and IBA. Endogenous NO was detected by the specific fluorescence probe 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate. SNP- and IBA-induced NO fluorescence was specifically suppressed by cPTIO. Nitrate reductase (NR) inhibitor sodium tungstate completely inhibited IBA-induced LR formation and NO fluorescence. However, nitric oxide synthase inhibitor N                         (G)-nitro-L: -arginine methyl ester hydrochloride slightly reduced IBA-induced LR formation and NO generation. It appears that NO generation that occurs in response to IBA might primarily involve NR activity. Moreover, NO production caused by SNP and IBA was localized in root area corresponding to LR emergence. The effects of Ca(2+) chelators, Ca(2+)-channel inhibitors, and calmodulin antagonists on LR formation induced by SNP and IBA were also examined. All these inhibitors were effective in reducing the action of SNP and IBA. However, Ca(2+) chelators and Ca(2+)-channel inhibitors had no effect on SNP- and IBA-induced NO generation. It is concluded that cytosolic levels of Ca(2+) may regulate SNP and IBA action through calmodulin-dependent mechanism.
authors.affiliation: Department of Agronomy, National Taiwan University, Taipei, Taiwan, Republic of China.
authors.forename: Yi Hsuan
authors.initials: YH
authors.lastname: Chen
authors.forename: Ching Huei
authors.initials: CH
authors.lastname: Kao
mesh_terms: D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001565:Benzoates / Q000494:pharmacology; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002147:Calmodulin / Q000037:antagonists & inhibitors; D002470:Cell Survival; D002614:Chelating Agents / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004789:Enzyme Activation; D005452:Fluoresceins / Q000378:metabolism; D007093:Imidazoles / Q000494:pharmacology; D007210:Indoleacetic Acids / Q000494:pharmacology*; D007211:Indoles / Q000494:pharmacology; D009565:Nitrate Reductases / Q000037:antagonists & inhibitors / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase; D009599:Nitroprusside / Q000494:pharmacology; D012275:Oryza / Q000187:drug effects* / Q000378:metabolism; D018517:Plant Roots / Q000187:drug effects* / Q000378:metabolism; D036226:Seedlings / Q000187:drug effects / Q000378:metabolism; D017973:Tungsten Compounds / Q000494:pharmacology
chemical_list: C503301:4-amino-5-methylamino-2',7'-difluorofluorescein diacetate; D001565:Benzoates; D002121:Calcium Channel Blockers; D002147:Calmodulin; D002614:Chelating Agents; D005452:Fluoresceins; D007093:Imidazoles; D007210:Indoleacetic Acids; D007211:Indoles; D017973:Tungsten Compounds; C014612:indolebutyric acid; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; C079393:1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole; D009599:Nitroprusside; C026512:arginine methyl ester; D009569:Nitric Oxide; D004533:Egtazic Acid; C025399:sodium tungstate(VI); D001120:Arginine; D019001:Nitric Oxide Synthase; D009565:Nitrate Reductases; D002118:Calcium