RESUMO
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 ribosome 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 preferentially 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 corroborated 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.
Assuntos
Medicago truncatula/genética , Estresse Oxidativo/efeitos dos fármacos , Ozônio/farmacologia , Biossíntese de Proteínas/efeitos dos fármacos , Metabolismo Energético , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Medicago truncatula/efeitos dos fármacos , Medicago truncatula/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Espécies Reativas de Oxigênio/metabolismoRESUMO
The action site of Alternaria alternata Crofton-weed toxin (AAC-toxin), isolated first from Alternaria alternata (Fr.) Keissler, was investigated in Chlamydomonas reinhardtii thylakoids. The results revealed that AAC-toxin inhibited photophosphorylation in a concentration-dependent pattern. Similarly, toxin inhibited uncoupled, basal electron flow and photosystem II (PSII) electron transport as well. However, toxin did not affect photosystem I (PSI) activity or the partial reaction of electron transport from H2O to silicomolybdic acid (SiMo). Therefore, the action site of toxin was located at QB level. In addition, the toxin may behave as an energy-transfer inhibitor at high concentrations by inhibiting phosphorylating electron transport and Mg2+ATPase activity. Chlorophyll a fluorescence induction and JIP test corroborated the inhibition at QB level. Through observations of the different sensitivity of toxin on D1 mutants of C. reinhardtii, evidence further confirmed that AAC-toxin inhibited electron transport by displacing the QB on the D1 protein, and the mode of action was similar to phenol-type PSII inhibitors.
