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bioRxiv · 10.1101/2020.12.17.423225

Single amino acid exchange in ACTIN2 confers increased tolerance to oxidative stress in Arabidopsis der1-3 mutant

Abstract

Single-point mutation in the ACTIN2 gene of der1-3 mutant revealed that ACTIN2 is an essential actin isovariant required for root hair tip growth, and leads to shorter, thinner and more randomly oriented actin filaments in comparison to wild-type C24 genotype. Actin cytoskeleton has been linked to plant defence against oxidative stress, but it is not clear how altered structural organization and dynamics of actin filaments may help plants to cope with oxidative stress. In this study, we characterized seed germination, root growth, plant biomass, actin organization and antioxidant activity of der1-3 mutant under oxidative stress induced by paraquat and H2O2. Under these conditions, plant growth was better in der1-3 mutant, while actin cytoskeleton in der1-3 carrying pro35S::GFP:FABD2 construct showed lower bundling rate and higher dynamicity. Biochemical analyses documented lower degree of lipid peroxidation, elevated capacity to decompose superoxide and hydrogen peroxide. These results support the view that der1-3 mutant is more resistant to oxidative stress. Single amino acid exchange in mutated ACTIN2 protein (Cys to Arg at the position 97) is topologically exposed to the protein surface and we propose that this might alter protein post-translational modifications and/or protein-protein interactions, leading to enhanced tolerance of der1-3 mutant against oxidative stress. HighlightTopological position of one amino acid exchanged in the ACTIN2 protein structure in der1-3 mutant enhanced tolerance to oxidative stress through increased capacity to decompose reactive oxygen species, lower bundling and enhanced dynamicity of the actin cytoskeleton.

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BibTeXRIS

Kubenova, L., Takac, T., Samaj, J., Ovecka, M.. 2020-12-18. Single amino acid exchange in ACTIN2 confers increased tolerance to oxidative stress in Arabidopsis der1-3 mutant. https://doi.org/10.1101/2020.12.17.423225

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