The roles of redox processes in pea nodule development and senescence

Nodule senescence is triggered by developmental and environmental cues. It is orchestrated through complex but poorly characterized genetic controls that involve changes in the endogenous levels of reactive oxygen species (ROS) and antioxidants. To elucidate the importance of such redox control mechanisms in pea root nodule senescence, redox metabolites were analysed throughout nodule development in a commercial pea variety (Pisum sativum cv. Phoenix) inoculated with a commercial rhizobial strain (Rhizobium leguminosarum bv. viciae). Although a strong positive correlation between nitrogenase activity and nodule ascorbate and glutathione contents was observed, the progressive loss of these metabolites during nodule senescence was not accompanied by an increase in nodule superoxide or hydrogen peroxide. These oxidants were only detected in nodule meristem and cortex tissues, and the abundance of superoxide or hydrogen peroxide strongly declined with age. No evidence could be found of programmed cell death in nodule senescence and the protein carbonyl groups were more or less constant throughout nodule development. Pea nodules appear to have little capacity to synthesize ascorbate de novo. L-galactono-1, 4-lactone dehydrogenase (GalLDH), which catalyses the last step of ascorbate synthesis could not be detected in nodules. Moreover, when infiltrated with the substrates L-galactono-1, 4-lactone or L-gulonolactone, ascorbate did not accumulate. These data suggest that ROS, ascorbate and glutathione, which fulfil well recognized, signalling functions in plants, decline in a regulated manner during nodule development. This does not necessarily cause oxidative stress but rather indicates a development-related shift in redox-linked metabolite cross-talk that underpins the development and aging processes.