Effects Of Elevated CO₂and Short-term Heat Stress On Physiological And Biochemical Variables In Maize Seedlings

To further systematically explore the photosynthetic physiology and biochemistry in response to short-term high temperature under elevated CO2in maize seedlings, this dissertation based on different chapters in turn were stretched out as following text,(1) Examine the high temperature threshold that can induce complete reverse of photosynthesis maintaining intact leave phenotypes. Focus on botanical characteristic and photosynthetic variables in response to different CO2levels for maize seedlings during growth period, to understand which traits exhibited acclimation to elevated CO2.(2) A hypothesis to prove stomatal conduct ances and transpiration increased with vapour pressure deficit and high temperature stress could be mitigated via elevated CO2effects on pore patern and water status, plants were subjected to combination of heat stress treatments and four CO2conditions (3) To further analysis on effects of CO2on phototysnthetic thermotolerance, plants were grown at indoor chambers and field. This study tested weather elevated CO2have modification on different maize cultivars that have contrasting thermotolerance in terms of photosynthetic variable and water status. Based on primary technical system and theory base, the study analyzed vitro activities of C4key photosynthetic enzymes, their transcriptional abundance, and integrity of cellular membrane.(4) to explore stressed-protein involved disruption and repairing by abiotic stress. Further test cellular metabolic reprogramming in response to heat stress and CO2effects was done. Based technical base and methods, this dissertation concluded as below:(1) High temperature45℃induced the decrease of photosynthesis, and was the best candidate temperature for abiostic temperature for obvious recovery after heat stress24h. There was no difference between2h and4h regarding the decrease of photosynthesis. This study investigated the interactive effects of heat treated time and CO2. Elevated CO2has no significance effects on root, stem and leaves, but enhanced leaf areas of maize seedlings, especially for B76(28.8%). SQ has fast growth developments. Activities of NADP-MDH increased under elevated CO2. Activities of NADP-MDH increased20%and31.6%for B76and SQ under elevated CO2. The activities of PEPCase decreased under elevated CO2.(2) Elevated CO2cannot mitigate the water potential during heat stress to protect the damage of photosynthesis. Effects of different CO2on photosynthetic thermotolerance have no significance difference. Heat treatment eliminated CO2effects. When leaf temperature recovered to35℃, gs and Ci maintained similar or higher values than initial values.(3) An opposite performances of photosynthetic tolerance was observed between field and indoor conditions. While under indoor, B76has more tolerance to heat stress. But under field conditions, photosynthetic tolerance was decreasing rather than B106. Transpiration and stomatal conductances performed opposite trends. Under field conditions, high temperature decreased transpiration and stomatal condutances rather than indoor conditions. Elevated CO2decreased the transpiration and stomatal conductances of B76, improving water potential of leaves as well as tolerance to heat stress. Heat stress induced relative injuries of B106were higher than B76suggesting B106has lower thermostability of cellular membrane. Activates of PEPCase and its gene expression were upregulated. But each heat shock protein has no CO2effects. Heat stress induced250times upregulation of HSP70expression in SQ,66.7%higher than B106at same conditions. In B76, the patterns of Hsp101and Hsp82have correlation with photosynthesis.(4) Under heat stress, total non-structural carbonhydrates decreased in all of maize cultivars. According to metabolic analysis, CO2enrichments increased25metabolites in B76. Under two CO2treatments, pyruvic acids and malic acids were influenced by heat treatments, suggesting the decrease of photosynthesis in B76probably was attributed to disruption of TCA cycles. Heat stress induced lectine, glycine, serine, proline, glutamate, fructose and glucose as well as decrease of isolectine, valine, aspirate and starch.