Induction of the AOX1D Isoform of Alternative Oxidase in A-thaliana T-DNA Insertion Lines Lacking Isoform AOX1A Is Insufficient to Optimize Photosynthesis when Treated with Antimycin A

Autor(en): Strodtkoetter, Inga
Padmasree, Kollipara
Dinakar, Challabathula
Speth, Birgit
Niazi, Pamela S.
Wojtera, Joanna
Voss, Ingo
Do, Phuc Thi
Nunes-Nesi, Adriano
Fernie, Alisdair R.
Linke, Vera
Raghavendra, Agepati S.
Scheibe, Renate 
Stichwörter: abiotic; acclimation-025EFphysiological; alternative electron transport; Biochemistry & Molecular Biology; CARBON ASSIMILATION; COMPLEX-I; DARK RESPIRATION; ELECTRON-TRANSPORT; environmental stress; MESOPHYLL PROTOPLASTS; mitochondria; MITOCHONDRIAL OXIDATIVE-METABOLISM; photorespiration; photosynthesis; Plant Sciences; PLANT-MITOCHONDRIA; RESPIRATORY-CHAIN; T-DNA insertion line; UNCOUPLING PROTEIN; UP-REGULATION
Erscheinungsdatum: 2009
Herausgeber: CELL PRESS
Volumen: 2
Ausgabe: 2
Startseite: 284
Seitenende: 297
Plant respiration is characterized by two pathways for electron transfer to O-2, namely the cytochrome pathway (CP) that is linked to ATP production, and the alternative pathway (AP), where electrons from ubiquinol are directly transferred to O-2 via an alternative oxidase (AOX) without concomitant ATP production. This latter pathway is well suited to dispose of excess electrons in the light, leading to optimized photosynthetic performance. We have characterized T-DNA-insertion mutant lines of Arabidopsis thaliana that do not express the major isoform, AOX1A. In standard growth conditions, these plants did not show any phenotype, but restriction of electron flow through CP by antimycin A, which induces AOX1A expression in the wild-type, led to an increased expression of AOX1D in leaves of the aox1a-knockout mutant. Despite the increased presence of the AOX1D isoform in the mutant, antimycin A caused inhibition of photosynthesis, increased ROS, and ultimately resulted in amplified membrane leakage and necrosis when compared to the wild-type, which was only marginally affected by the inhibitor. It thus appears that AOX1D was unable to fully compensate for the loss of AOX1A when electron flow via the CP is restricted. A combination of inhibition studies, coupled to metabolite profiling and targeted expression analysis of the P-protein of glycine decarboxylase complex (GDC), suggests that the aox1a mutants attempt to increase their capacity for photorespiration. However, given their deficiency, it is intriguing that increase in expression neither of AOX1D nor of GDC could fully compensate for the lack of AOX1A to optimize photosynthesis when treated with antimycin A. We suggest that the aox1a mutants can further be used to substantiate the current models concerning the influence of mitochondrial redox on photosynthetic performance and gene expression.
ISSN: 16742052
DOI: 10.1093/mp/ssn089

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