摘要
Plants glycerol-3-phosphate dehydrogenase(GPDH)catalyzes the formation of glycerol-3-phosphate,and plays an essential role in glycerolipid metabolism and stress responses.In the present study,the knock-out mutants of cytosolic GPDH(AtGPDHc2)and wild-type Arabidopsis plants were treated with 0,50,100,and 150 mmol L–1 NaCl to reveal the effects of AtGPDHc2 deficiency on salinity stress responses.The fluctuation in redox status,reactive oxygen species(ROS)and antioxidant enzymes as well as the transcripts of genes involved in the relevant processes were measured.In the presence of 100 and 150 mmol L–1 NaCl treatments,AtGPDHc2-deficient plants exhibited a pronounced reduction in germination rate,fresh weight,root length,and overall biomass.Furthermore,loss of AtGPDHc2 resulted in a significant perturbation in cellular redox state(NADH/NAD+and AsA/DHA)and consequent elevation of ROS and thiobarbituric acid-reactive substances(TBARS)content.The elevated ROS level triggered substantial increases in ROS-scavenging enzymes activities,and the up-regulated transcripts of the genes(CSD1,sAPX and PER33)encoding the antioxidant enzymes were also observed.In addition,the transcript levels of COX15,AOX1A and GLDH in gpdhc2 mutants decreased in comparison to wild-type plants,which demonstrated that the deficiency of AtGPDHc2 might also has impact on mitochondrial respiration under salt stress.Together,this work provides some new evidences on illustrating the roles of AtGPDHc2 playing in response to salinity stress by regulating cellular redox homeostasis,ROS metabolism and mitochondrial respiration.
Plants glycerol-3-phosphate dehydrogenase(GPDH) catalyzes the formation of glycerol-3-phosphate, and plays an essential role in glycerolipid metabolism and stress responses. In the present study, the knock-out mutants of cytosolic GPDH(AtGPDHc2) and wild-type Arabidopsis plants were treated with 0, 50, 100, and 150 mmol L–1 NaCl to reveal the effects of AtGPDHc2 deficiency on salinity stress responses. The fluctuation in redox status, reactive oxygen species(ROS) and antioxidant enzymes as well as the transcripts of genes involved in the relevant processes were measured. In the presence of 100 and 150 mmol L–1 NaCl treatments, AtGPDHc2-deficient plants exhibited a pronounced reduction in germination rate, fresh weight, root length, and overall biomass. Furthermore, loss of AtGPDHc2 resulted in a significant perturbation in cellular redox state(NADH/NAD+ and AsA/DHA) and consequent elevation of ROS and thiobarbituric acid-reactive substances(TBARS) content. The elevated ROS level triggered substantial increases in ROS-scavenging enzymes activities, and the up-regulated transcripts of the genes(CSD1, sAPX and PER33) encoding the antioxidant enzymes were also observed. In addition, the transcript levels of COX15, AOX1 A and GLDH in gpdhc2 mutants decreased in comparison to wild-type plants, which demonstrated that the deficiency of AtGPDHc2 might also has impact on mitochondrial respiration under salt stress. Together, this work provides some new evidences on illustrating the roles of At GPDHc2 playing in response to salinity stress by regulating cellular redox homeostasis, ROS metabolism and mitochondrial respiration.
基金
supported by the National Key Research and Development Program of China (2016YFD0101002)
the Heilongjiang Bayi Agricultural University Scientific Start-up Found for the Returned Overseas Chinese Scholar (2031011047)
the Heilongjiang Bayi Agricultural University Key Cultivating Program, China (XA2014-01)
