Abstract
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 thaliana frostbite1 (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.
Highlights
Plants are autotrophic organisms that use assimilated nitrogen and carbon for the biosynthesis of proteins and other organic compounds in order to fulfil the developmental needs of their organs
Characterization of fro1 Plants Cultured on Different Nitrogen Sources
The consequences of limited ability to oxidize cellular oxidants in mutants carrying a point mutation in NDUFS4 (AT5G67590), affecting complex I assembly—frostbite1 [46,47], on plant growth was observed under NH4+ and NO3− nutrition
Summary
Plants are autotrophic organisms that use assimilated nitrogen and carbon for the biosynthesis of proteins and other organic compounds in order to fulfil the developmental needs of their organs. Research using complex I mutants indicates that complex I defects in plants are compensated by reorganization of respiration, oxidative phosphorylation rates are not fully restored, and most mutant plants are energy deficient Because of their altered metabolic status, most complex I mutants examined so far showed retarded growth and developmental disorders, in comparison to wild-type (WT) plants. The fro mutation reduced the expression of stress-inducible genes during chilling conditions, which impaired cold acclimation, whereby mutants became sensitive to other stress factors like NaCl and osmotic stress [46] In contrast to these responses, in our recent study, fro plants showed improved resistance to ammonium nutrition [47]. The role of plant mitochondria in retrograde signalling and PCD was analyzed
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have