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Mitochondrial complex I dysfunction increases CO 2 efflux and reconfigures metabolic fluxes of day respiration in tobacco leaves
Author(s) -
Lothier Jérémy,
De Paepe Rosine,
Tcherkez Guillaume
Publication year - 2019
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.15393
Subject(s) - biology , biochemistry , metabolism , mutant , catabolism , citric acid cycle , respiration , efflux , electron transport chain , cellular respiration , metabolic pathway , respiratory chain , mitochondrion , botany , gene
Summary Mutants affected in complex I are useful to understand the role played by mitochondrial electron transport and redox metabolism in cellular homeostasis and signaling. However, their respiratory phenotype is incompletely described and a specific examination of day respiration ( R d ) is lacking. Here, we used isotopic methods and metabolomics to investigate the impact of complex I dysfunction on R d in two respiratory mutants of forest tobacco ( Nicotiana sylvestris ): cytoplasmic male sterile II (CMSII) and nuclear male sterile 1 (NMS1), previously characterized for complex I disruption. R d was higher in mutants and the inhibition of leaf respiration by light was lower. Higher R d values were caused by increased (phospho enol )pyruvate (PEP) metabolism at the expense of anaplerotic (PEP carboxylase (PEPc) ‐catalyzed) activity. De novo synthesis of Krebs cycle intermediates in the light was larger in mutants than in the wild‐type, although numerically small in all genotypes. Carbon metabolism in mutants involved alternative pathways, such as alanine synthesis, and an increase in amino acid production with the notable exception of aspartate. Our results show that the alteration of NADH re‐oxidation activity by complex I does not cause a general inhibition of catabolism, but rather a re‐orchestration of fluxes in day respiratory metabolism, leading to an increased CO 2 efflux.