Nitric oxide production occurs downstream of reactive oxygen species in guard cells during stomatal closure induced by chitosan in abaxial epidermis of Pisum sativum.
The effects of chitosan (beta-1,4 linked glucosamine, a fungal elicitor), on the patterns of stomatal movement and signaling components were studied. cPTIO (NO scavenger), sodium tungstate (nitrate reductase inhibitor) or L: -NAME (NO synthase inhibitor) restricted the chitosan induced stomatal closure, demonstrating that NO is an essential factor. Similarly, catalase (H(2)O(2) scavenger) or DPI [NAD(P)H oxidase inhibitor] and BAPTA-AM or BAPTA (calcium chelators) prevented chitosan induced stomatal closure, suggesting that reactive oxygen species (ROS) and calcium were involved during such response. Monitoring the NO and ROS production in guard cells by fluorescent probes (DAF-2DA and H(2)DCFDA) indicated that on exposure to chitosan, the levels of NO rose after only 10 min, while those of ROS increased already by 5 min. cPTIO or sodium tungstate or L: -NAME prevented the rise in NO levels but did not restrict the ROS production. In contrast, catalase or DPI restricted the chitosan-induced production of both ROS and NO in guard cells. The calcium chelators, BAPTA-AM or BAPTA, did not have a significant effect on the chitosan induced rise in NO or ROS. We propose that the production of NO is an important signaling component and participates downstream of ROS production. The effects of chitosan strike a marked similarity with those of ABA or MJ on guard cells and indicate the convergence of their signal transduction pathways leading to stomatal closure.
Srivastava
Nupur
N
Department of Plant Sciences, School of Life Sciences, University of Hyderabad, Hyderabad, 500046, India.
Gonugunta
Vijay K
VK
Puli
Mallikarjuna R
MR
Raghavendra
Agepati S
AS
D000040:Abscisic Acid / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D048271:Chitosan / Q000494:pharmacology*; D003497:Cyclic N-Oxides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D016166:Free Radical Scavengers / Q000494:pharmacology; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D007700:Kinetics; D018613:Microscopy, Confocal; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009861:Onium Compounds / Q000494:pharmacology; D016877:Oxidants / Q000494:pharmacology; D018532:Pisum sativum / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D019441:Plant Epidermis / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010937:Plant Growth Regulators / Q000494:pharmacology; D054046:Plant Stomata / Q000187:drug effects* / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013997:Time Factors; D017973:Tungsten Compounds / Q000494:pharmacology
D002614:Chelating Agents; D003497:Cyclic N-Oxides; D004791:Enzyme Inhibitors; D016166:Free Radical Scavengers; D007093:Imidazoles; D009861:Onium Compounds; D016877:Oxidants; D010937:Plant Growth Regulators; D017382:Reactive Oxygen Species; D017973:Tungsten Compounds; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; C079391:2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide; D009569:Nitric Oxide; D004533:Egtazic Acid; C025399:sodium tungstate(VI); C007517:diphenyleneiodonium; D000040:Abscisic Acid; D048271:Chitosan; D006861:Hydrogen Peroxide; D019001:Nitric Oxide Synthase; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D019331:NG-Nitroarginine Methyl Ester