Complex I impairment, respiratory compensations, and photosynthetic decrease in nuclear and mitochondrial male sterile mutants of Nicotiana sylvestris

We have previously shown that in Nicotiana sylzsylvestris cytoplasmic male- sterile (CMS) mutants where the mtDNA lacks the nad7 gene coding fur a subu nit of respiratory Complex I (NADH:ubiquinone oxidoreductase, EC 1.6.5.3), glycine (Gly) oxidation was lower than in the wild type and insensitive to rotenone, suggesting Complex I dysfunction. In contrast, the oxidation rate of exogenous NADII and the capacity of the cyanide-resistant respiration ( AOX) were enhanced. Here we rep report that , in contrast to Gly, the rate of malate oxidation was not affected, but proceeded totally in a rotenone-i nsensitive pathway, strongly suggesting that survival of CMS plants depends on the activation of internal and external alternative NAD(P) H dehydrogen ases and that Gly decarboxylase activity depends on Complex I functioning. A similar defect in Complex I activity and Gly oxidation was found in the N MS1 nuclear mutant, defective in the processing of the nad4 transcript, but alternative NAD(P) H dehydrogenases were less activated. In CMS and NMS1, the fraction of the AOX pathway was increased, as compared to wild type, as sociated with higher amounts of aox transcripts, AOX protein, and plant res istance to cyanide. Non-phosphorylating respiratory enzymes maintained norm al in vivo respiration levels in both mutants, but photosynthesis was decre ased, in correlation with lower leaf conductance, emphasizing mitochondrial control on photosynthesis.