Mitochondrial complex I dysfunction increases CO2 efflux and reconfigures metabolic fluxes of day respiration in tobacco leaves. Issue 2 (22nd August 2018)

• Record Type: Journal Article
• Authors: Lothier, Jérémy; De Paepe, Rosine; Tcherkez, Guillaume
• Is Part Of: New phytologist. Volume 221:Issue 2(2019)
• Page Start: 750
• Page End: 763
• Publication Date: 2018-08-22
• Subjects: CO2 efflux -- day respiration (Rd) -- isotopic labeling -- photorespiration -- tricarboxylic acid cycle; Botany -- Periodicals; 580
• DOI: 10.1111/nph.15393
• Languages: English
• ISSNs: 0028-646X

Abstract

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 CO2 efflux.