Identification of a Plant Nitric Oxide Synthase Gene Involved in Hormonal Signaling

Guo, Fang‐Qing; Okamoto, Mamoru; Crawford, Nigel M.

doi:10.1126/science.1086770

Cited by 801 publications

(835 citation statements)

References 20 publications

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“…To further characterize the source of NO during Cd 2+ treatment, similar experiments were performed in the atnoa1 mutant impaired in the expression of the AtNOA1 gene encoding an enzyme initially thought to catalyze NO synthesis from L-Arg (Crawford et al, 2006;Moreau et al, 2008). The mutant atnoa1 was reported to be impaired in NO synthesis or accumulation in response to abscisic acid or lipopolysaccharide treatments (Guo et al, 2003;Zeidler et al, 2004). Our data indicate that the Cd 2+ -induced NO synthesis was not suppressed in atnoa1 (Fig.…”

Section: Resultsmentioning

confidence: 57%

Nitric Oxide Contributes to Cadmium Toxicity in Arabidopsis by Promoting Cadmium Accumulation in Roots and by Up-Regulating Genes Related to Iron Uptake

et al. 2009

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Nitric oxide (NO) functions as a cell-signaling molecule in plants. In particular, a role for NO in the regulation of iron homeostasis and in the plant response to toxic metals has been proposed. Here, we investigated the synthesis and the role of NO in plants exposed to cadmium (Cd 2+ ), a nonessential and toxic metal. We demonstrate that Cd 2+ induces NO synthesis in roots and leaves of Arabidopsis (Arabidopsis thaliana) seedlings. This production, which is sensitive to NO synthase inhibitors, does not involve nitrate reductase and AtNOA1 but requires IRT1, encoding a major plasma membrane transporter for iron but also Cd 2+ . By analyzing the incidence of NO scavenging or inhibition of its synthesis during Cd 2+ treatment, we demonstrated that NO contributes to Cd 2+ -triggered inhibition of root growth. To understand the mechanisms underlying this process, a microarray analysis was performed in order to identify NO-modulated root genes up-and down-regulated during Cd 2+ treatment. Forty-three genes were identified encoding proteins related to iron homeostasis, proteolysis, nitrogen assimilation/metabolism, and root growth. These genes include IRT1. Investigation of the metal and ion contents in Cd 2+ -treated roots in which NO synthesis was impaired indicates that IRT1 up-regulation by NO was consistently correlated to NO's ability to promote Cd 2+ accumulation in roots. This analysis also highlights that NO is responsible for Cd 2+ -induced inhibition of root Ca 2+ accumulation. Taken together, our results suggest that NO contributes to Cd 2+ toxicity by favoring Cd 2+ versus Ca 2+ uptake and by initiating a cellular pathway resembling those activated upon iron deprivation.

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Section: Resultsmentioning

confidence: 57%

Nitric Oxide Contributes to Cadmium Toxicity in Arabidopsis by Promoting Cadmium Accumulation in Roots and by Up-Regulating Genes Related to Iron Uptake

et al. 2009

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“…The released fragment was used to replace the original GFP-RNAi fragment in the pX7-GFP binary vector to produce pX7-APY1. The pX7-GFP binary vector and pSKint were provided by Dr. Nam-Hai Chua (Rockefeller University; Guo et al, 2003). The pX7-APY1 binary vector was electroporated into A. tumefaciens strain GV3101.…”

Section: Generation Of the Rnai Construct And Plant Transformationmentioning

confidence: 99%

Apyrases (Nucleoside Triphosphate-Diphosphohydrolases) Play a Key Role in Growth Control in Arabidopsis

et al. 2007

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Expression of two Arabidopsis (Arabidopsis thaliana) apyrase (nucleoside triphosphate-diphosphohydrolase) genes with high similarity, APY1 and APY2, was analyzed during seedling development and under different light treatments using b-glucuronidase fusion constructs with the promoters of both genes. As evaluated by b-glucuronidase staining and independently confirmed by other methods, the highest expression of both apyrases was in rapidly growing tissues and/or tissues that accumulate high auxin levels. Red-light treatment of etiolated seedlings suppressed the protein and message level of both apyrases at least as rapidly as it inhibited hypocotyl growth. Adult apy1 and apy2 single mutants had near-normal growth, but apy1apy2 doubleknockout plants were dwarf, due primarily to reduced cell elongation. Pollen tubes and etiolated hypocotyls overexpressing an apyrase had faster growth rates than wild-type plants. Growing pollen tubes released ATP into the growth medium and suppression of apyrase activity by antiapyrase antibodies or by inhibitors simultaneously increased medium ATP levels and inhibited pollen tube growth. These results imply that APY1 and APY2, like their homologs in animals, act to reduce the concentration of extracellular nucleotides, and that this function is important for the regulation of growth in Arabidopsis.

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“…It is well known that a variety of second messengers contribute to the transmission of the ABA signal, which includes Ca 21 , cADP-Rib, reactive oxygen species, nitric oxide, phosphoinositides, phosphatidic acid, and sphingosine 1-P (Schroeder and Hagiwara, 1989;Gilroy et al, 1990;McAinsh et al, 1990;Wu et al, 1997;Leckie et al, 1998;Jacob et al, 1999;Lemtiri-Chlieh et al, 2000;Pei et al, 2000;Allen et al, 2001;Ng et al, 2001;Neill et al, 2002;Guo et al, 2003). It is also known that phosphorylation/dephosphorylation events play a crucial role in ABA signaling, which involves a complex network of protein kinases and phosphatases as well as other signal transducers (for review, see Finkelstein et al, 2002).…”

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confidence: 99%

Enhancement of Abscisic Acid Sensitivity and Reduction of Water Consumption in Arabidopsis by Combined Inactivation of the Protein Phosphatases Type 2C ABI1 and HAB1

et al. 2006

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Abscisic acid (ABA) plays a key role in plant responses to abiotic stress, particularly drought stress. A wide number of ABAhypersensitive mutants is known, however, only a few of them resist/avoid drought stress. In this work we have generated ABA-hypersensitive drought-avoidant mutants by simultaneous inactivation of two negative regulators of ABA signaling, i.e. the protein phosphatases type 2C (PP2Cs) ABA-INSENSITIVE1 (ABI1) and HYPERSENSITIVE TO ABA1 (HAB1). Two new recessive loss-of-function alleles of ABI1, abi1-2 and abi1-3, were identified in an Arabidopsis (Arabidopsis thaliana) T-DNA collection. These mutants showed enhanced responses to ABA both in seed and vegetative tissues, but only a limited effect on plant drought avoidance. In contrast, generation of double hab1-1 abi1-2 and hab1-1 abi1-3 mutants strongly increased plant responsiveness to ABA. Thus, both hab1-1 abi1-2 and hab1-1 abi1-3 were particularly sensitive to ABA-mediated inhibition of seed germination. Additionally, vegetative responses to ABA were reinforced in the double mutants, which showed a strong hypersensitivity to ABA in growth assays, stomatal closure, and induction of ABA-responsive genes. Transpirational water loss under drought conditions was noticeably reduced in the double mutants as compared to single parental mutants, which resulted in reduced water consumption of whole plants. Taken together, these results reveal cooperative negative regulation of ABA signaling by ABI1 and HAB1 and suggest that fine tuning of ABA signaling can be attained through combined action of PP2Cs. Finally, these results suggest that combined inactivation of specific PP2Cs involved in ABA signaling could provide an approach for improving crop performance under drought stress conditions.

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Identification of a Plant Nitric Oxide Synthase Gene Involved in Hormonal Signaling

Cited by 801 publications

References 20 publications

Nitric Oxide Contributes to Cadmium Toxicity in Arabidopsis by Promoting Cadmium Accumulation in Roots and by Up-Regulating Genes Related to Iron Uptake

Nitric Oxide Contributes to Cadmium Toxicity in Arabidopsis by Promoting Cadmium Accumulation in Roots and by Up-Regulating Genes Related to Iron Uptake

Apyrases (Nucleoside Triphosphate-Diphosphohydrolases) Play a Key Role in Growth Control in Arabidopsis

Enhancement of Abscisic Acid Sensitivity and Reduction of Water Consumption in Arabidopsis by Combined Inactivation of the Protein Phosphatases Type 2C ABI1 and HAB1

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