Nitric oxide, stomatal closure and abiotic stress
Neill, S., Barros, R. S., Bright, J., Desikan, R., Hancock, J. T., Harrison, J., Morris, P. and Ribeiro, D. M. (2007) Nitric oxide, stomatal closure and abiotic stress. Comparative Biochemistry and Physiology - Part A: Molecular & Integrative Physiology, 146 (4). S257. ISSN 1095-6433 Available from: http://eprints.uwe.ac.uk/7098
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Publisher's URL: http://dx.doi.org/10.1016/j.cbpa.2007.01.648
Various data indicate that nitric oxide (NO) is an endogenous signal in plants that mediates responses to several stimuli. Experimental evidence in support of such signalling roles for NO has been obtained via the application of NO (usually in the form of NO donors), via the measurement of endogenous NO and through the manipulation of endogenous NO content via chemical and genetic means. Stomatal closure initiated by abscisic acid (ABA) is effected through a complex symphony of intracellular signalling in which NO appears to be one component. Exogenous NO induces stomatal closure, ABA triggers NO generation, removal of NO by an NO scavenger inhibits stomatal closure in response to ABA and ABA-induced stomatal closure is reduced in mutants that have impaired NO generation. The data indicate that ABA-induced guard cell NO generation requires both a nitric oxide synthase-like activity and, in Arabidopsis, nitrate reductase (NR), in particular NR1. NO stimulates both MAP kinase activity and cGMP production, both of which are required for ABA-induced stomatal closure.Data from other laboratories suggest that drought and salinity stress can induce NO generation, and that NO could activate cellular processes that afford some protection against these stresses. Cellular responses to NO may differ depending on the NO concentration; at higher concentrations NO can cause stomatal opening and may be toxic. Our data for Arabidopsis indicate that responses to NO differ between wilting and turgid tissue and suggest that guard cell responses in planta reflect complex interactions between hormonal and redox signalling.