Transcriptional Regulation of Hydrogen Peroxide and Calcium for Signaling Transduction and Stress-defensive Genes Contributing to Improved Drought Tolerance in Creeping Bentgrass

Small molecules, including H2O2 and Ca, mediate stress signaling and drought tolerance in plants. The objective of this study was to determine whether improvement in drought tolerance by H2O2 and Ca were associated with the regulation of transcription factors and stress-protective genes in perennial grass species. Plants of creeping bentgrass (Agrostis stolonifera) were sprayed with water (control), H2O2 (9 mm), or CaCl2 (10 mm) and exposed to drought stress for 20 days in controlled-environment growth chambers. Foliar application of H2O2 or Ca led to significant improvement in drought tolerance of creeping bentgrass, as demonstrated by greater turf quality, leaf relative water content, chlorophyll content, photochemical efficiency, and cell membrane stability, as compared with the untreated control. The application of H2O2 and Ca resulted in significant up-regulation of genes in Ca signaling transduction pathways [Ca-dependent kinase 26 (CDPK26), mitogen-activated protein kinase 1 (MAPK1), and 14-3-3] and transcript factors (WRKY75 and MYB13). For genes encoding antioxidant enzymes, H2O2 mainly enhanced superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and dehydroascorbate reductase (DHAR) expression, while Ca primarily improved transcript levels of SOD, monodehydroascorbate reductase (MDHAR), and GR. In addition, heat shock protein 70 (HSP70), metallothionein 1 (MT1), and glutamine synthetase 2 (GS2) were also markedly up-regulated by H2O2 and Ca under drought stress. However, the transcript level of lipoxygenase 3 (LOX3) was significantly down-regulated by H2O2 and Ca under well-watered and drought conditions. These results imply that H2O2 and Ca commonly or differentially regulate genes expression in association with drought tolerance through activating Ca signaling pathway and regulating transcription factors and stress-protective genes expression, leading to the alleviation of lipid peroxidation, maintenance of correct protein folding and translocation, and enhancement of nitrogen metabolism under a prolonged period of drought stress in creeping bentgrass.

Stimulation of fibroblast growth factor 23 by metabolic acidosis requires osteoblastic intracellular calcium signaling and prostaglandin synthesis

Serum fibroblast growth factor 23 (FGF23) increases progressively in chronic kidney disease (CKD) and is associated with increased mortality. FGF23 is synthesized in osteoblasts and osteocytes; however, the factors regulating its production are not clear. Patients with CKD have decreased renal acid excretion leading to metabolic acidosis (MET). During MET, acid is buffered by bone with release of mineral calcium (Ca) and phosphate (P). MET increases intracellular Ca signaling and cyclooxygenase 2 (COX2)-induced prostaglandin production in the osteoblast, leading to decreased bone formation and increased bone resorption. We found that MET directly stimulates FGF23 in mouse bone organ cultures and primary osteoblasts. We hypothesized that MET increases FGF23 through similar pathways that lead to bone resorption. Neonatal mouse calvariae were incubated in neutral (NTL, pH = 7.44, Pco2 = 38 mmHg, [HCO3−] = 27 mM) or acid (MET, pH = 7.18, Pco2 = 37 mmHg, [HCO3−] = 13 mM) medium without or with 2-APB (50 μM), an inhibitor of intracellular Ca signaling or NS-398 (1 μM), an inhibitor of COX2. Each agent significantly inhibited MET stimulation of medium FGF23 protein and calvarial FGF23 RNA as well as bone resorption at 48 h. To exclude the potential contribution of MET-induced bone P release, we utilized primary calvarial osteoblasts. In these cells each agent inhibited MET stimulation of FGF23 RNA expression at 6 h. Thus stimulation of FGF23 by MET in mouse osteoblasts utilizes the same initial signaling pathways as MET-induced bone resorption. Therapeutic interventions directed toward correction of MET, especially in CKD, have the potential to not only prevent bone resorption but also lower FGF23 and perhaps decrease mortality.

The role of luminal Ca regulation in Ca signaling refractoriness and cardiac arrhythmogenesis

Györke et al. discuss the role of sarcoplasmic reticulum Ca2+ in cardiac refractoriness and pathological implications.