Abstract
Synergistic interaction of nitric oxide (NO) and reactive oxygen species (ROS) is essential to initiate cell death mechanisms in plants. Though autophagy is salient in either restricting or promoting hypersensitivity response (HR)-related cell death, the crosstalk between the reactive intermediates and autophagy during hypersensitivity response is paradoxical. In this investigation, the consequences of Alternaria alternata toxin (AaT) in tobacco BY-2 cells were examined. At 3 h, AaT perturbed intracellular ROS homeostasis, altered antioxidant enzyme activities, triggered mitochondrial depolarization and induced autophagy. Suppression of autophagy by 3-Methyladenine caused a decline in cell viability in AaT treated cells, which indicated the vital role of autophagy in cell survival. After 24 h, AaT facilitated Ca2+ influx with an accumulation of reactive oxidant intermediates and NO, to manifest necrotic cell death. Inhibition of NO accumulation by 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) decreased the level of necrotic cell death, and induced autophagy, which suggests NO accumulation represses autophagy and facilitates necrotic cell death at 24 h. Application of N-acetyl-L-cysteine at 3 h, confirmed ROS to be the key initiator of autophagy, and together with cPTIO for 24 h, revealed the combined effects of NO and ROS is required for necrotic HR cell death.
Highlights
Through the course of their lifespan, plants encounter numerous pathogenic invasions, and mount multilayered intrinsic programs to combat such attacks
Loss of cytoplasmic extent with a significant increase in the volume occupied by lytic vacuoles, invagination and fusion of vacuolar membranes with vesicles for subsequent cargo degradation and eventually tonoplast rupture, and discharge of vacuolar hydrolases can be assigned as autophagic cell death markers[21]
We report a thorough evaluation of alternata toxin (AaT)-incited intracellular consequences in terms of altered calcium ion (Ca2+) concentration, accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), evaluation of redox balance in terms of reduced and oxidized glutathione ratio (GSH/GSSG), mitochondrial depolarization, antioxidant profile, autophagy and toxin-induced cell death, in cultured wild-type and transgenic BY-2 cells expressing GFP-Atg[8] protein
Summary
Through the course of their lifespan, plants encounter numerous pathogenic invasions, and mount multilayered intrinsic programs to combat such attacks. In Nicotiana tabacum (tobacco), the pathogen has been reported to inculcate lethal symptoms like anthracnose, black root rot, frog eye leaf spot, verticillium wilt and brown spots Among these diseases, brown spot predominantly engenders more than 50 per cent depletion in global tobacco production[31]. The cytotoxic A. alternata extract[35] further purified to obtain crude toxin[36], activated caspase-like proteases and induced reactive oxygen species (ROS) but no DNA fragmentation (the hallmark feature of apoptosis). Contrary to this observation Cheng et al.[37] reported A. alternata metabolic extract-induced apoptosis-like PCD in tobacco BY-2 cells. A thorough exploration of A. alternata toxin (AaT)-induced disruption of cellular homoeostasis and cell death as a consequence of HR is absent
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