Abstract

Single-point mutation in the ACTIN2 gene of the 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 the wild-type C24 genotype. The actin cytoskeleton has been linked to plant defense 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 root growth, plant biomass, actin organization and antioxidant activity of the der1–3 mutant under oxidative stress induced by paraquat and H2O2. Under these conditions, plant growth was better in the der1–3 mutant, while the actin cytoskeleton in the der1–3 carrying pro35S::GFP:FABD2 construct showed a lower bundling rate and higher dynamicity. Biochemical analyses documented a lower degree of lipid peroxidation, and an elevated capacity to decompose superoxide and hydrogen peroxide. These results support the view that the der1–3 mutant is more resistant to oxidative stress. We propose that alterations in the actin cytoskeleton, increased sensitivity of ACTIN to reducing agent dithiothreitol (DTT), along with the increased capacity to decompose reactive oxygen species encourage the enhanced tolerance of this mutant against oxidative stress.

Highlights

  • Plants are continuously exposed to fluctuating environmental conditions, including adverse biotic and abiotic stressors

  • Arabidopsis thaliana mutant der1–3 has been produced in the C24 ecotype background by an ethylmethanesulfonic acid-induced mutagenesis in the DER1 locus, leading to a single-point mutation in the ACTIN2 gene [42]

  • We found that this position, both in the natural (Figure 1A) and mutated (Figure 1B) ACTIN2 protein is placed in a loop located at the protein periphery (Videos S1 and S2)

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Summary

Introduction

Plants are continuously exposed to fluctuating environmental conditions, including adverse biotic and abiotic stressors. Alone or in combination with other stress factors, may disrupt the cellular homeostasis in plants. ROS serve as signaling molecules, playing important roles in the regulation of numerous plant developmental processes [1,2,3], they are generated as toxic by-products of the aerobic metabolism under stress conditions [4,5,6,7,8]. The production of ROS with metabolic or stress-related origin, is controlled by components of redox signaling pathways. These maintain cellular ROS homeostasis, since both low and high ROS levels are undesirable for plant cells. An equilibrated threshold of ROS is maintained and controlled by the activity of antioxidant enzymes from the family of superoxide dismutases (SODs), catalases, peroxidases, gluthatione peroxidases, iron uptake/storage regulating proteins, and a network of thio- and glutaredoxins [8,9,10]

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