cyclic-gmp and 1-aminocyclopropane-1-carboxylic-acid

cGMP promotes ethylene production and enhances the perception of ethylene. Endogenous ethylene or cGMP accumulation maintains ion homeostasis to enhancing salt resistance. etr1 - 3 is insensitive to cGMP under salt stress.. In the present study, we presented a signaling network involving ethylene and cGMP in salt resistance pathway of Arabidopsis roots. Results showed that the ethylene-insensitive mutant etr1-3 was more sensitive to salt stress than the wild type (WT). etr1-3 displayed a greater electrolyte leakage, thiobarbituric acid reactive substances and Na(+)/K(+) ratio, but a lower plasma membrane (PM) H(+)-ATPase activity compared to WT under the different NaCl contents. Application of 1-aminocyclopropane-1-carboxylic acid (ACC, an ethylene precursor) or 8-Br-cGMP (the cGMP analog) alleviated NaCl-induced injury by maintaining a lower Na(+)/K(+) ratio and increasing PM H(+)-ATPase activity in WT, but not in etr1-3. Roots treated with 8-Br-cGMP could promote ethylene production and enhance the expression of ACC synthase gene in WT. In addition, the 8-Br-cGMP action in NaCl stress was inhibited by aminooxyacetic acid (an inhibitor of ethylene biosynthesis), but 6-Anilino-5,8-quinolinedione (Ly83583, a guanylate cyclase inhibitor) could not affect ACC action in WT. These results suggest that ethylene functions as a downstream signal of cGMP that stimulates the PM H(+)-ATPase activity, which finally results in regulating ion homeostasis in Arabidopsis tolerance to salt. Moreover, cGMP enhanced the perception of ethylene in Arabidopsis under salt stress, which reversed the salt-induced increase of ETR1 and increased ERF1 at the transcript levels in WT. In a word, cGMP modulates salt resistance pathway of ethylene through regulating biosynthesis and perception of ethylene in Arabidopsis roots.

Topics: Amino Acids, Cyclic; Arabidopsis; Cyclic GMP; Ethylenes; Ions; Plant Roots; Sodium Chloride

Partial agonists at the strychnine-insensitive glycine sites coupled to N-methyl-D-aspartate (NMDA) receptors reduce both glutamate-induced neurotoxicity in vitro and ischemia-induced neurodegeneration in vivo. Paradoxically, sustained exposure of cultured cerebellar granule cell neurons to glycinergic ligands, including glycine and the glycine partial agonists (+/-)-3-amino-1-hydroxy-2-pyrrolidone, 1-aminocyclopropanecarboxylic acid (ACPC), and D-cycloserine, attenuates the neuroprotective effects of (+/-)-3-amino-1-hydroxy-2-pyrrolidone and ACPC. In the present study, we investigated the mechanisms responsible for this attenuated neuroprotection. Three NMDA receptor-mediated responses were examined after sustained exposure to ACPC: glutamate-induced neurotoxicity, NMDA-stimulated increases in cGMP levels, and NMDA-stimulated increases in [Ca+2]i. Consistent with previous findings, coincubation with ACPC blocked glutamate-induced neurotoxicity, whereas sustained (24 hr) exposure to ACPC attenuated its protective effects. Moreover, sustained exposure to ACPC caused an apparent approximately 2-fold increase in the potency of both glutamate to act as neurotoxin and NMDA to stimulate cGMP formation. Sustained exposure to ACPC also increased NMDA-stimulated [Ca+2]i approximately 3-fold compared with control granule cell cultures but did not affect basal [Ca+2]i. This apparent increase in glutamate sensitivity may be attributable to a change in NMDA receptor subunit composition as sustained ACPC exposure resulted in a approximately 2.5-fold increase in NMDA receptor 2C RNA levels, without concomitant changes in the amounts of RNA encoding the NMDA receptor 2A, 2B, or 1 subunit. This is the first demonstration that sustained exposure to a glycinergic ligand can alter the expression of RNAs encoding NMDA receptor subunits. Because glycinergic ligands are potential clinical candidates, these results may have important implications for the treatment of neurodegenerative disorders.

Topics: Amino Acids; Amino Acids, Cyclic; Animals; Calcium; Cell Death; Cerebellum; Cyclic GMP; Cytoplasmic Granules; Drug Synergism; Glutamic Acid; Glycine; Macromolecular Substances; Mice; N-Methylaspartate; Neurons; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; RNA; Stimulation, Chemical