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Mitochondrial complex I dysfunction increases CO₂ efflux and reconfigures metabolic fluxes of day respiration in tobacco leaves

Lothier, Jeremy; De Paepe, Rosine; Tcherkez, Guillaume

Description

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 (Rd) is lacking. Here, we used isotopic methods and metabolomics to investigate the impact of complex I dysfunction on Rd in two respiratory mutants of forest tobacco (Nicotiana sylvestris): cytoplasmic male sterile II...[Show more]

dc.contributor.authorLothier, Jeremy
dc.contributor.authorDe Paepe, Rosine
dc.contributor.authorTcherkez, Guillaume
dc.date.accessioned2019-08-27T01:36:23Z
dc.identifier.issn0028-646X
dc.identifier.urihttp://hdl.handle.net/1885/165227
dc.description.abstractMutants 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 (Rd) is lacking. Here, we used isotopic methods and metabolomics to investigate the impact of complex I dysfunction on Rd 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. Rd was higher in mutants and the inhibition of leaf respiration by light was lower. Higher Rd values were caused by increased (phosphoenol)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.
dc.format.mimetypeapplication/pdf
dc.language.isoen_AU
dc.publisherWiley
dc.rights© 2018 The Author(s) © 2018 New Phytologist Trust
dc.sourceNew Phytologist
dc.titleMitochondrial complex I dysfunction increases CO₂ efflux and reconfigures metabolic fluxes of day respiration in tobacco leaves
dc.typeJournal article
local.description.notesImported from ARIES
local.identifier.citationvolume221
dc.date.issued2019
local.identifier.absfor060705 - Plant Physiology
local.identifier.ariespublicationu3102795xPUB302
local.publisher.urlhttps://www.wiley.com/en-gb
local.type.statusPublished Version
local.contributor.affiliationLothier, Jeremy, Universite d’Angers
local.contributor.affiliationDe Paepe, Rosine, Universite Paris-Sud XI
local.contributor.affiliationTcherkez, Guillaume, College of Science, ANU
local.description.embargo2037-12-31
dc.relationhttp://purl.org/au-research/grants/arc/FT140100645
local.bibliographicCitation.issue2
local.bibliographicCitation.startpage750
local.bibliographicCitation.lastpage763
local.identifier.doi10.1111/nph.15393
local.identifier.absseo970106 - Expanding Knowledge in the Biological Sciences
dc.date.updated2019-04-14T08:25:39Z
local.identifier.scopusID2-s2.0-85052541606
CollectionsANU Research Publications

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