摘要
Acute ozone is a model abiotic elicitor of oxidative stress and a useful tool for understanding biochemical and molecular events during oxidative signaling. Two Medicago truncatula accessions with contrasting responses to ozone were used to examine translational regulation during ozone stress. In ozone-resistant JE154, significant reduction in ri- bosome loading was observed within one hour of ozone treatment, suggesting energy homeostasis as a vital factor for oxidative stress management. Polysomal RNA-based expression profiling with Affymetrix arrays revealed extensive changes in the translatomes of both accessions. Messenger RNAs with low GC content in their 5＇ and 3＇-UTRs were pref- erentially associated with polysomes during oxidative stress. Genebins analysis revealed extensive changes in various gene ontologies in both accessions. Extensive changes in nicotinate and nicotinamide metabolism genes were corrobo- rated with increased levels of NAD＋ and NADH in JE154. The significantly lower NAD＋：NADH redox status in JE154, in conjunction with higher ATP amounts, provided a cellular milieu conducive for overcoming oxidative stress. Low levels of ATP, NADH, and suppression of antioxidant defense responses, abet build-up of ozone-derived ROS and ultimately lead to oxidative cell death in Jemalong.
Acute ozone is a model abiotic elicitor of oxidative stress and a useful tool for understanding biochemical and molecular events during oxidative signaling. Two Medicago truncatula accessions with contrasting responses to ozone were used to examine translational regulation during ozone stress. In ozone-resistant JE154, significant reduction in ri- bosome loading was observed within one hour of ozone treatment, suggesting energy homeostasis as a vital factor for oxidative stress management. Polysomal RNA-based expression profiling with Affymetrix arrays revealed extensive changes in the translatomes of both accessions. Messenger RNAs with low GC content in their 5＇ and 3＇-UTRs were pref- erentially associated with polysomes during oxidative stress. Genebins analysis revealed extensive changes in various gene ontologies in both accessions. Extensive changes in nicotinate and nicotinamide metabolism genes were corrobo- rated with increased levels of NAD＋ and NADH in JE154. The significantly lower NAD＋：NADH redox status in JE154, in conjunction with higher ATP amounts, provided a cellular milieu conducive for overcoming oxidative stress. Low levels of ATP, NADH, and suppression of antioxidant defense responses, abet build-up of ozone-derived ROS and ultimately lead to oxidative cell death in Jemalong.
