Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.7.1.2 (nitrate reductase)
 3,861 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO) is a gas with crucial signaling functions in plant defense and development. As demonstrated by generating a triple nia1nia2noa1-2 mutant with extremely low levels of NO (February 2010 issue of Plant Physiology), NO is synthesized in plants through mainly two different pathways involving nitrate reductase (NR/NIA) and NO Associated 1 (AtNOA1) proteins. Depletion of basal NO levels leads to a priming of ABA-triggered responses that causes hypersensitivity to this hormone and results in enhanced seed dormancy and decreased seed germination and seedling establishment in the triple mutant. NO produced under non-stressed conditions represses inhibition of seed developmental transitions by ABA. Moreover, NO plays a positive role in post-germinative vegetative development and also exerts a critical control of ABA-related functions on stomata closure. The triple nia1nia2noa1-2 mutant is hypersensitive to ABA in stomatal closure thus resulting in a extreme phenotype of resistance to drought. In the light of the recent discovery of PYR/PYL/RCAR as a family of potential ABA receptors, regulation of ABA sensitivity by NO may be exerted either directly on ABA receptors or on downstream signaling components; both two aspects that deserve our present and future attention.
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PMID:Nitric oxide modulates sensitivity to ABA. 2000 48

Sugars play important roles in regulating plant growth, development, and stomatal movement. Here, we found that glucose triggered stomatal closure in a dose- and time-dependent manner in Arabidopsis. Pharmacological data showed that glucose-induced stomatal closure was greatly inhibited by catalase [CAT; a reactive oxygen species (ROS) scavenger], diphenyleneiodonium chloride (DPI; an NADPH oxidase inhibitor), lanthanum chloride (LaCl3; a Ca2+ channel blocker), EGTA (a Ca2+ chelator), and two nitrate reductase (NR) inhibitors, tungstate and sodium azide (NaN3), while it was not affected by salicylhydroxamic acid (SHAM; a peroxidase inhibitor). Moreover, glucose induced ROS and nitric oxide (NO) production in guard cells of Arabidopsis. The ROS production was almost completely removed by CAT, strongly restricted by DPI, and was not affected by SHAM. NO production was partially suppressed by tungstate and NaN3, and the levels of NO were significantly reduced in the nia1-1nia2-5 mutant. Additionally, glucose-triggered stomatal closure was significantly impaired in gin1-1, gin2-1, pyr1pyl1pyl2pyl4, abi1-1, ost1, slac1-4, cpk6-1, and nia1-1nia2-5 mutants. Likewise, the reductions in leaf stomatal conductance (gs) and transpiration rate (E) caused by glucose were reversed in the above mutants. These results suggest that glucose-triggered stomatal closure may be dependent on basal signaling through PYR/RCAR receptors and hexokinase1 (HXK1).
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PMID:Glucose triggers stomatal closure mediated by basal signaling through HXK1 and PYR/RCAR receptors in Arabidopsis. 2944 16