For optimal plant growth, carbon and nitrogen availability needs to be tightly coordinated. Mitochondrial perturbations related to a defect in complex I in the Arabidopsis thalianafrostbite1 (fro1) mutant, carrying a point mutation in the 8-kD Fe-S subunit of NDUFS4 protein, alter aspects of fundamental carbon metabolism, which is manifested as stunted growth. During nitrate nutrition, fro1 plants showed a dominant sugar flux toward nitrogen assimilation and energy production, whereas cellulose integration in the cell wall was restricted. However, when cultured on NH₄⁺ as the sole nitrogen source, which typically induces developmental disorders in plants (i.e., the ammonium toxicity syndrome), fro1 showed improved growth as compared to NO₃- nourishing. Higher energy availability in fro1 plants was correlated with restored cell wall assembly during NH₄⁺ growth. To determine the relationship between mitochondrial complex I disassembly and cell wall-related processes, aspects of cell wall integrity and sugar and reactive oxygen species signaling were analyzed in fro1 plants. The responses of fro1 plants to NH₄⁺ treatment were consistent with the inhibition of a form of programmed cell death. Resistance of fro1 plants to NH₄⁺ toxicity coincided with an absence of necrotic lesion in plant leaves.
Keywords: NDUFS4; cell wall synthesis; complex I defect; frostbite1; mitochondrial mutant; necrosis; programmed cell death; reactive oxygen species; sugar catabolism; sugar signaling.