NADPH oxidase is involved in regulation of gene expression and ROS overproduction in soybean (Glycine max L.) seedlings exposed to cadmium

Jagna Chmielowska-Bąk,Magdalena Arasimowicz-Jelonek,Inga Zinicovscaia,Karolina Izbiańska,Joanna Deckert,Carolina Guiance-Varela,Marina Frontasyeva

doi:10.5586/asbp.3551

Abstract

Cadmium-induced oxidative burst is partially mediated by NADPH oxidase. The aim of the present research was to evaluate the role of NADPH oxidase in soybeans’ response to short-term cadmium stress. The application of an NADPH oxidase inhibitor, diphenyleneiodonium chloride (DPI), affected expression of two Cd-inducible genes, encoding DOF1 and MYBZ2 transcription factors. This effect was observed after 3 h of treatment. Interestingly, Cd-dependent increases in NADPH oxidase activity occurred only after a period of time ranging from 6 and 24 h of stress. Stimulation of the enzyme correlated in time with a significant accumulation of reactive oxygen species (ROS). Further analysis revealed that pharmacological inhibition of NADPH oxidase activity during 24 h of Cd stress does not affect Cd uptake, seedling growth, or the level of lipid peroxidation. The role of NADPH oxidase in the response of soybean seedlings to short-term Cd exposure is discussed.

Highlights

Contamination of the environment with Cd is a serious problem in many parts of the world [1,2]
6 h-long exposure to Cd led to the stimulation of the genes encoding 1-aminocyclopropane-1-carboxylate synthase (ACS), nitrate reductase (NR), and MYBZ2 and bZIP62 transcription factors (Fig. 1e–h)
In the case of the control, treatment with diphenyleneiodonium chloride (DPI) resulted in elevated expression of the gene encoding DOF1 transcription factor after 3 h of exposure and attenuation of the expression of acid synthase (ACS), NR, and MYBZ2 genes after 6 h

Summary

Introduction

Contamination of the environment with Cd is a serious problem in many parts of the world [1,2]. This heavy metal exhibits toxic effects in all organisms. In the case of plants, exposure to Cd leads to oxidative stress, lipid peroxidation, DNA damage, changes in protein structure and their function, and degradation of photosynthetic pigments. These toxicity mechanisms result in alterations in photosynthesis, imbalances in ion homeostasis, impeded cell division, growth inhibition, and eventually cell death [3,4]. There are several sources of ROS in Cd-stressed plants, including alterations in mitochondria functioning, depletion of the antioxidant system, and increased activity in the membrane-bound, O2−-producing enzyme NADPH oxidase, with the latter being

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