4.7 Article

The role of the electron-transfer flavoprotein: ubiquinone oxidoreductase following carbohydrate starvation in Arabidopsis cell cultures

期刊

PLANT CELL REPORTS
卷 41, 期 2, 页码 431-446

出版社

SPRINGER
DOI: 10.1007/s00299-021-02822-1

关键词

Alternative respiration; Branched-chain amino acids; Carbon starvation; ETF; ETFQO systems; Mitochondria

资金

  1. binational science funding program 'PROBRAL' of the Deutsche Akademische Austauschdienst (DAAD by the Bundesministerium fur Bildung und Forschung-BMBF)
  2. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [423/14]
  3. National Council for Scientific and Technological Development (CNPq-Brazil)

向作者/读者索取更多资源

This study investigates the impact of the functional absence of ETFQO on cell respiration and enzyme activity in Arabidopsis thaliana. The results suggest that while the absence of ETFQO affects specific enzyme activity, it does not have a major impact on cell respiration, possibly due to alternative pathways.
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.

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