TY - JOUR

T1 - The role of the electron-transfer flavoprotein

T2 - ubiquinone oxidoreductase following carbohydrate starvation in Arabidopsis cell cultures

AU - Brito, Danielle S

AU - Quinhones, Carla G S

AU - Neri-Silva, Roberto

AU - Heinemann, Björn

AU - Schertl, Peter

AU - Cavalcanti, João Henrique F

AU - Eubel, Holger

AU - Hildebrandt, Tatjana

AU - Nunes-Nesi, Adriano

AU - Braun, Hans-Peter

AU - Araújo, Wagner L

N1 - Funding Information: We would like to thank Prof. Dr. Christoph Peterhänsel (Leibniz Universität Hannover) for kindly providing physical space in her laboratory and access to equipment for performing parts of this research project. We gratefully acknowledge Christa Ruppelt, Dagmar Lewejohann, and Marianne Langer for excellent technical assistance as well as Professor Samuel Martins (Universidade Federal de Vicosa) for his support with the statistics. This work was supported by the binational science funding program ‘PROBRAL’ of the Deutsche Akademische Austauschdienst (DAAD; funds provided by the Bundesministerium für Bildung und Forschung—BMBF) and the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Refs: Project-ID PROBRAL #423/14. Furthermore, research fellowships granted by the National Council for Scientific and Technological Development (CNPq-Brazil) to ANN and WLA are gratefully acknowledged.

PY - 2022/2

Y1 - 2022/2

N2 - KEY MESSAGE: The functional absence of the electron-transfer flavoprotein: ubiquinone oxidoreductase (ETFQO) directly impacts electrons donation to the mitochondrial electron transport chain under carbohydrate-limiting conditions without major impacts on the respiration of cell cultures. Alternative substrates (e.g., amino acids) can directly feed electrons into the mitochondrial electron transport chain (mETC) via the electron transfer flavoprotein/electron-transfer flavoprotein: ubiquinone oxidoreductase (ETF/ETFQO) complex, which supports plant respiration during stress situations. By using a cell culture system, here we investigated the responses of Arabidopsis thaliana mutants deficient in the expression of ETFQO (etfqo-1) following carbon limitation and supplied with amino acids. Our results demonstrate that isovaleryl-CoA dehydrogenase (IVDH) activity was induced during carbon limitation only in wild-type and that these changes occurred concomit with enhanced protein content. By contrast, neither the activity nor the total amount of IVDH was altered in etfqo-1 mutants. We also demonstrate that the activities of mitochondrial complexes in etfqo-1 mutants, display a similar pattern as in wild-type cells. Our findings suggest that the defect of ETFQO protein culminates with an impaired functioning of the IVDH, since no induction of IVDH activity was observed. However, the functional absence of the ETFQO seems not to cause major impacts on plant respiration under carbon limiting conditions, most likely due to other alternative electron entry pathways.

AB - KEY MESSAGE: The functional absence of the electron-transfer flavoprotein: ubiquinone oxidoreductase (ETFQO) directly impacts electrons donation to the mitochondrial electron transport chain under carbohydrate-limiting conditions without major impacts on the respiration of cell cultures. Alternative substrates (e.g., amino acids) can directly feed electrons into the mitochondrial electron transport chain (mETC) via the electron transfer flavoprotein/electron-transfer flavoprotein: ubiquinone oxidoreductase (ETF/ETFQO) complex, which supports plant respiration during stress situations. By using a cell culture system, here we investigated the responses of Arabidopsis thaliana mutants deficient in the expression of ETFQO (etfqo-1) following carbon limitation and supplied with amino acids. Our results demonstrate that isovaleryl-CoA dehydrogenase (IVDH) activity was induced during carbon limitation only in wild-type and that these changes occurred concomit with enhanced protein content. By contrast, neither the activity nor the total amount of IVDH was altered in etfqo-1 mutants. We also demonstrate that the activities of mitochondrial complexes in etfqo-1 mutants, display a similar pattern as in wild-type cells. Our findings suggest that the defect of ETFQO protein culminates with an impaired functioning of the IVDH, since no induction of IVDH activity was observed. However, the functional absence of the ETFQO seems not to cause major impacts on plant respiration under carbon limiting conditions, most likely due to other alternative electron entry pathways.

KW - Alternative respiration

KW - Branched-chain amino acids

KW - Carbon starvation

KW - ETF/ETFQO systems

KW - Mitochondria

UR - http://www.scopus.com/inward/record.url?scp=85123069048&partnerID=8YFLogxK

U2 - 10.1007/s00299-021-02822-1

DO - 10.1007/s00299-021-02822-1

M3 - Article

C2 - 35031834

VL - 41

SP - 431

EP - 446

JO - Plant cell reports

JF - Plant cell reports

SN - 0721-085X

IS - 2

ER -