Evidence map›Paper›PMID 26134164›Full record

ArticlePlant physiology2015

Complete Mitochondrial Complex I Deficiency Induces an Up-Regulation of Respiratory Fluxes That Is Abolished by Traces of Functional Complex I.

Kristina Kühn, Toshihiro Obata, Kristen Feher, Ralph Bock, Alisdair R Fernie, Etienne H Meyer

Open access · hybridAbstract read
In one paragraph

Article in Plant physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 119 citations in OpenAlex.

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  15. Transcriptional and metabolomic responses ofFrontiers in microbiology · 2023
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  17. Mitochondrial DNA Isolation from Plants.Methods in molecular biology (Clifton, N.J.) · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Kristina KühnMolekulare Zellbiologie der Pflanzen, Humboldt-Universität zu Berlin, 10115 Berlin, Germany (K.K.);Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 67084 Strasbourg, France (K.K., E.H.M.); andMax-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Potsdam-Golm, Germany (T.O., K.F., R.B., A.R.F., E.H.M.).ORCID http://orcid.org/0000-0001-6747-783X
Toshihiro ObataMolekulare Zellbiologie der Pflanzen, Humboldt-Universität zu Berlin, 10115 Berlin, Germany (K.K.);Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 67084 Strasbourg, France (K.K., E.H.M.); andMax-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Potsdam-Golm, Germany (T.O., K.F., R.B., A.R.F., E.H.M.).ORCID http://orcid.org/0000-0001-8931-7722
Kristen FeherMolekulare Zellbiologie der Pflanzen, Humboldt-Universität zu Berlin, 10115 Berlin, Germany (K.K.);Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 67084 Strasbourg, France (K.K., E.H.M.); andMax-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Potsdam-Golm, Germany (T.O., K.F., R.B., A.R.F., E.H.M.).
Ralph BockMolekulare Zellbiologie der Pflanzen, Humboldt-Universität zu Berlin, 10115 Berlin, Germany (K.K.);Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 67084 Strasbourg, France (K.K., E.H.M.); andMax-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Potsdam-Golm, Germany (T.O., K.F., R.B., A.R.F., E.H.M.).ORCID http://orcid.org/0000-0001-7502-6940
Alisdair R FernieMolekulare Zellbiologie der Pflanzen, Humboldt-Universität zu Berlin, 10115 Berlin, Germany (K.K.);Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 67084 Strasbourg, France (K.K., E.H.M.); andMax-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Potsdam-Golm, Germany (T.O., K.F., R.B., A.R.F., E.H.M.).
Etienne H MeyerMolekulare Zellbiologie der Pflanzen, Humboldt-Universität zu Berlin, 10115 Berlin, Germany (K.K.);Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, 67084 Strasbourg, France (K.K., E.H.M.); andMax-Planck-Institut für Molekulare Pflanzenphysiologie, 14476 Potsdam-Golm, Germany (T.O., K.F., R.B., A.R.F., E.H.M.) emeyer@mpimp-golm.mpg.de.ORCID http://orcid.org/0000-0003-4712-9824
Max Planck Institute of Molecular Plant Physiology · DEHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complex I (NADH:ubiquinone oxidoreductase) is central to cellular NAD(+) recycling and accounts for approximately 40% of mitochondrial ATP production. To understand how complex I function impacts respiration and plant development, we isolated Arabidopsis (Arabidopsis thaliana) lines that lack complex I activity due to the absence of the catalytic subunit NDUFV1 (for NADH:ubiquinone oxidoreductase flavoprotein1) and compared these plants with ndufs4 (for NADH:ubiquinone oxidoreductase Fe-S protein4) mutants possessing trace amounts of complex I. Unlike ndufs4 plants, ndufv1 lines were largely unable to establish seedlings in the absence of externally supplied sucrose. Measurements of mitochondrial respiration and ATP synthesis revealed that compared with ndufv1, the complex I amounts retained by ndufs4 did not increase mitochondrial respiration and oxidative phosphorylation capacities. No major differences were seen in the mitochondrial proteomes, cellular metabolomes, or transcriptomes between ndufv1 and ndufs4. The analysis of fluxes through the respiratory pathway revealed that in ndufv1, fluxes through glycolysis and the tricarboxylic acid cycle were dramatically increased compared with ndufs4, which showed near wild-type-like fluxes. This indicates that the strong growth defects seen for plants lacking complex I originate from a switch in the metabolic mode of mitochondria and an up-regulation of respiratory fluxes. Partial reversion of these phenotypes when traces of active complex I are present suggests that complex I is essential for plant development and likely acts as a negative regulator of respiratory fluxes.

Indexed as

MutationAdenosine TriphosphateArabidopsisArabidopsis ProteinsElectron Transport Complex IElectrophoresis, Polyacrylamide GelGene Expression ProfilingGene Expression Regulation, DevelopmentalGene Expression Regulation, PlantMitochondriaOligonucleotide Array Sequence AnalysisOxygen ConsumptionPhenotypePlant LeavesReverse Transcriptase Polymerase Chain ReactionSeedlingsAdenosine TriphosphateArabidopsis ProteinsElectron Transport Complex INDUFS4 protein, Arabidopsis

Identifiers

PMID26134164
PMCPMC4528760
OpenAlexW1931712295

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.