Phospholipase D activation is required for 1-aminocyclopropane 1-carboxylic acid signaling during sexual reproduction in the marine red alga Neopyropia yezoensis (Rhodophyta).

BACKGROUND: 1-aminocyclopropane 1-carboxylic acid (ACC) is the immediate precursor of the plant hormone ethylene. However, recent studies have suggested that ACC also acts as a signaling molecule to regulate development and growth independently from ethylene biosynthesis. In red algae, ACC stimulates the switch from a vegetative to a sexual reproductive phase. However, despite evidence that ACC signaling in plants and algae is widespread, the mechanistic basis of the ACC signaling pathway remains unknown. RESULTS: We demonstrate that exogenous ACC increased the activity of phospholipase D (PLD) and induced the accumulation of PLD transcripts in the marine red alga Neopyropia yezoensis. The product of PLD, the lipid second messenger phosphatidic acid (PA), also increased in response to ACC. Furthermore, the pharmacological inhibition of PLD by 1-butanol blocked ACC-induced spermatangia and carpospore production, but the inactive isomer t-butanol did not. In addition, 1-butanol prevented ACC-induced growth inhibition and inhibited transcript accumulation of genes upregulated by ACC, including extracellular matrix (ECM)-related genes, and alleviated the transcriptional decrease of genes downregulated by ACC, including photosynthesis-related genes. CONCLUSIONS: These results indicate that PLD is a positive regulator of sexual cell differentiation and a negative regulator of growth. This study demonstrates that PLD and its product, PA, are components of ACC signaling during sexual reproduction in N. yezoensis.

Selective downregulation of N-methyl-D-aspartate receptor (NMDAR) rather than non-NMDAR subunits in ipsilateral cerebral hemispheres in rats with middle cerebral artery occlusion.

Ischemic brain damage is believed to involve the drastic increase in extracellular glutamate levels after reperfusion and subsequent overactivation of both N-methyl-D-aspartate (NMDA) receptor (NMDAR) and non-NMDAR channels for delayed neuronal cell death mediated by Ca2+ overload. In this study, we evaluated expression profiles of mRNA and corresponding proteins for different subunits of NMDAR and non-NMDAR in brains of rats with transient middle cerebral artery occlusion (MCAO). Cellular vitality was markedly reduced in proportion to increasing durations of MCAO for 1 to 8 h when determined 1 day after reperfusion. Within 7 days after reperfusion, MCAO for 2 h led to a gradual decrease in the neuronal marker microtubules-associated protein-2 (MAP2) level in the ipsilateral cerebral hemisphere, in addition to inducing a transient increase in the microglial marker CD11b expression without affecting the astroglial marker protein levels. MCAO for 2 h significantly decreased the expression of both mRNA and corresponding proteins for NR1, NR2A and NR2B subunits of NMDAR, but not for non-NMDAR subunits, in the ipsilateral hemisphere. These results suggest that NMDAR may be preferentially down-regulated in response to ischemic signal inputs amongst three different subtypes of ionotropic glutamate receptors in rats with MCAO.