Mitochondrial redox state, nitrogen metabolism and signalling.

Nitrogen is often a limiting factor for plant growth and development, and therefore there is considerable interest and potential agronomic benefit not only in understanding the mechanisms that determine nitrogen use efficiency (NUE)but also in identifying new targets for NUE improvement. Much attention in recent years has focused on the core pathways and enzymes involved in primary nitrogen assimilation as well as the processes of N uptake and transport. However, recent studies on mitochondrial Complex I mutants indicate that enzymes involved in energy metabolism in the mitochondria could also be useful targets for improving NUE. The Nicotiana sylvestris cytoplasmic male sterile II (CMSII)mutant lacks respiratory Complex I, but high rates of respiration are sustained because of the presence of alternative NADH dehydrogenases. The CMSII mutation has striking effects on leaf amino acids, which are the focal point around which primary N assimilation and associated carbon metabolism and photorespiration and export occur, and on pyridine nucleotides, which are essential for metabolism and signalling. The absence of major mitochondrial NADH dehydrogenase (Complex I)in the CMSII mutant results in an N?rich phenotype and altered N signalling. Adjustments in the abundance of Complex I relative to the alternative NADH dehydrogenases could therefore provide a mechanism for improved NUE.