Highlights d Plants use a systemic root-shoot-root signaling loop to defend against nematodes d Nematode resistance is largely dependent on JA synthesis in shoots, but not in roots d Nematodes induce the systemic propagation of electrical signals d Interdependency of electrical and ROS signals results in the activation of MPK1/2
Elevated atmospheric CO2 improves leaf photosynthesis and plant tolerance to heat stress, however, the underlying mechanisms remain unclear. In this study, we exposed tomato plants to elevated CO2 (800 μmol mol-1) and/or high temperature (42°C for 24 h), and examined a range of photosynthetic and chlorophyll fluorescence parameters as well as cellular redox state to better understand the response of photosystem II (PSII) and PSI to elevated CO2 and heat stress. The results showed that, while the heat stress drastically decreased the net photosynthetic rate (Pn), maximum carboxylation rate (Vcmax), maximum ribulose-1,5-bis-phosphate (RuBP) regeneration rate (Jmax) and maximal photochemical efficiency of PSII (Fv/Fm), the elevated CO2 improved those parameters under heat stress and at a 24 h recovery. Furthermore, the heat stress decreased the absorption flux, trapped energy flux, electron transport, energy dissipation per PSII cross section, while the elevated CO2 had the opposing effects that eventually decreased photoinhibition, damage to photosystems and reactive oxygen species accumulation. Similarly, the elevated CO2 helped the plants to maintain a reduced redox state as evidenced by the increased ratios of ASA:DHA and GSH:GSSG under heat stress and at recovery. Furthermore, the concentration of NADP+ and ratio of NADP+ to NADPH were induced by elevated CO2 at recovery. This study unraveled the crucial mechanisms of elevated CO2-mediated changes in energy fluxes, electron transport and redox homeostasis under heat stress, and shed new light on the responses of tomato plants to combined heat and elevated CO2.
Despite being essential for C plants, photorespiration is believed to cause a significant crop yield loss even under future climates. However, how photorespiration affects plant basal defence still remains largely unknown. Here, we studied the involvement of photorespiration in tomato-Pseudomonas syringae pv. tomato DC3000 interaction focusing on three photorespiratory genes. Inoculation with P. syringae increased photorespiration rate (Pr) and expression of glycolate oxidase (GOX2), serine glyoxylate aminotransferase (SGT) and serine hydroxyl methyltransferase (SHMT1); however, inhibition of photorespiration by isonicotinic acid hydrazide decreased tomato basal defence against P. syringae. Furthermore, silencing of GOX2, SGT or SHMT1 genes in tomato decreased Pr but increased susceptibility to P. syringae, whereas transient overexpression of GOX2, SGT or SHMT1 in tobacco increased basal defence. Further study revealed that salicylic acid (SA) signalling is involved in GOX2-mediated, SGT-mediated and SHMT1-mediated defence. Moreover, H O pretreatment remarkably alleviated the GOX2 silencing-induced depression in basal defence and SA signalling, whereas it had no effect on that of SGT-silenced and SHMT1-silenced plants. Taken together, these results suggest that H O is critical for GOX2-modulated but not SGT-modulated or SHMT1-modulated SA signalling and subsequent basal defence against P. syringae. This work deepens the understanding of photorespiration-involved defence responses to bacterial attack in plants.
Climate changes such as heat waves often affect plant growth and pose a growing threat to natural and agricultural ecosystems. Elevated atmospheric CO can mitigate the negative effects of heat stress, but the underlying mechanisms remain largely unclear. We examined the interactive effects of elevated CO (eCO ) and temperature on the generation of the hydrogen peroxide (H O ) and stomatal movement characteristics associated with heat tolerance in tomato seedlings grown under two CO concentrations (400 and 800 µmol mol ) and two temperatures (25 and 42°C). eCO ameliorated the negative effects of heat stress, which was accompanied by greater amounts of RESPIRATORY BURST OXIDASE 1 (RBOH1) transcripts, apoplastic H O accumulation and decreased stomatal aperture. Silencing RBOH1 and SLOW-TYPE ANION CHANNEL, impeded eCO -induced stomatal closure and compromised the eCO -enhanced water use efficiency as well as the heat tolerance. Our findings suggest that RBOH1-dependent H O accumulation was involved in the eCO -induced stomatal closure, which participate in maintaining balance between water retention and heat loss under eCO concentrations. This phenomenon may be a contributor to eCO -induced heat tolerance in tomato, which will be critical for understanding how plants respond to both future climate extremes and changes in CO .
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