Light signaling and phytohormones both influence plant growth, development, and stress responses; however, cross talk between these two signaling pathways in response to cold remains underexplored. Here, we report that far-red light (FR) and red light (R) perceived by phytochrome A (phyA) and phyB positively and negatively regulated cold tolerance, respectively, in tomato (Solanum lycopersicum), which were associated with the regulation of levels of phytohormones such as abscisic acid (ABA) and jasmonic acid (JA) and transcript levels of ABA-and JA-related genes and the C-REPEAT BINDING FACTOR (CBF) stress signaling pathway genes. A reduction in the R/FR ratio did not alter cold tolerance, ABA and JA accumulation, and transcript levels of ABA-and JA-related genes and the CBF pathway genes in phyA mutant plants; however, those were significantly increased in wild-type and phyB plants with the reduction in the R/FR ratio. Even though low R/FR treatments did not confer cold tolerance in ABA-deficient (notabilis [not]) and JA-deficient (prosystemin-mediated responses2 [spr2]) mutants, it up-regulated ABA accumulation and signaling in the spr2 mutant, with no effect on JA levels and signaling in the not mutant. Foliar application of ABA and JA further confirmed that JA functioned downstream of ABA to activate the CBF pathway in light quality-mediated cold tolerance. It is concluded that phyA and phyB function antagonistically to regulate cold tolerance that essentially involves FR light-induced activation of phyA to induce ABA signaling and, subsequently, JA signaling, leading to an activation of the CBF pathway and a cold response in tomato plants.

Silencing the calcium-dependent protein kinase CPK27 in tomato decreases cold-induced ABA, H2O2 and NO production, as well as decreasing activation of mitogen-activated protein kinase, compromising cold acclimation.

Plant glutamate receptor-like (GLR) genes play important roles in plant development and immune response. However, the functions of GLRs in abiotic stress response remain unclear. Here we show that cold acclimation at 12°C induced the transcripts of GLR3.3 and GLR3.5 with increased tolerance against a subsequent chilling at 4°C. Silencing of GLR3.3 or/and GLR3.5 or application of the antagonist of ionotropic glutamate receptor 6,7-dinitroquinoxaline-2,3-dione (DNQX), all compromised the acclimation-induced increases in the transcripts of respiratory burst oxidase homolog1 (RBOH1), activity of NADPH oxidase, the accumulation of apoplastic H 2 O 2 and the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG), resulting in an attenuated chilling tolerance; the effect, however, was rescued by foliar application of H 2 O 2 or GSH. Both RBOH1-silenced and glutathione biosynthesis genes, γglutamylcysteine synthetase (GSH1)-and glutathione synthetase (GSH2)-cosilenced plants had decreased chilling tolerance with reduced GSH/GSSG ratio. Moreover, application of DNQX had little effects on the GSH/GSSG ratio and the tolerance in RBOH1-silenced plants and GSH1-and GSH2-cosilenced plants. These findings unmasked the functional hierarchy of GLR-H 2 O 2 -glutathione cascade and shed new light on cold response pathway in tomato plants.

HighlightHigh CO2 concentrations can counteract the negative impact of salt stress in an apoplastic H2O2-dependent manner by regulating stomatal movement and Na+ delivery from the xylem to leaf cells.