Chitosan elicited immune response reduces photosynthetic electron transport and ion channel activity in the guard cells of Vicia

It has been shown that a fungal elicitor chitosan (CHT) inhibits the blue light-induced stomatal opening and can trigger stomatal closure. These movements are related to the H+-ATPase activity in the guard cell (GC) plasma membrane that affects the transport of osmotically active solutes. The ATP for proton pumping is supplied mostly from mitochondrial respiration; however, a partial inhibition by DCMU implies a role of GC photosynthetic electron transport in the ATP supply. In order to investigate whether CHT affects the photosynthetic ATP production of Vicia GCs, the light-dependence of the photosynthetic electron transport rate (ETR) of individual GCs was assayed. In addition, to test the possible effect of CHT on the activity of ion channels, GC protoplasts were investigated by patch clamp technique

Involvement of nitric oxide (NO) in plant responses to metalloids

Plants respond to the limited or excess supply of metalloids, boron (B), silicon (Si), selenium (Se), arsenic (As), and antimony (Sb) via complex signaling pathways that are mainly regulated by nitric oxide (NO). The absorption of metalloids from the soil is facilitated by pathways that involve aquaporins, aquaglyceroporins, phosphate, and sulfate transporters; however, their regulation by NO is poorly understood. Using in silico software, we predicted the S-nitrosation of known metalloid transporters, proposing NO-dependent regulation of metalloid transport systems at the posttranslational level. NO intensifies the stress-mitigating effect of Si, whereas in the case of Se, As, and Sb, the accumulation of NO or reactive nitrogen species contributes to toxicity. NO promotes the beneficial effect of low Se concentrations and mitigates the damage caused by B deficiency. In addition, the exogenous application of NO donor, sodium nitroprusside, reduces B, Se, and As toxicity. The primary role of NO in metalloid stress response is to mitigate oxidative stress by activating antioxidant defense at the level of protein activity and gene expression. This review discusses the role of NO in plant responses to metalloids and suggests future research directions. © 2021 The Author

Investigating the role of potassium channel KAT1 in NO mediated stomatal closure

KAT1, a hyperpolarization-activated, inward-rectifying K+ channel is one of the main transportersparticipating in guard cell volume regulation. The voltage-dependence of KAT1 channel is regulated by several intracellular factors, including pH, ATP and cGMP (Hoshi 1995). NO, a regulator of a branch of ABA signalling pathways in guard cells decreases the Ca2+-dependent inward potassium current by increasing the cytosolic free Ca2+ concentration. Based on the Ca2+-independent feature of KAT1 homotetramer protein, we aimed to examine the direct and indirect effects of NO on this channel

Fusaric acid-evoked oxidative stress affects plant defence system by inducing biochemical changes at subcellular level

Fusaric acid (FA) is one of the most harmful phytotoxins produced in various plant–pathogen interactions. Fusarium species produce FA as a secondary metabolite, which can infect many agronomic crops at all stages of development from seed to fruit, and FA production can further compromise plant survival because of its phytotoxic effects. FA exposure in plant species adversely affects plant growth, development and crop yield. FA exposure in plants leads to the generation of reactive oxygen species (ROS), which cause cellular damage and ultimately cell death. Therefore, FA-induced ROS accumulation in plants has been a topic of interest for many researchers to understand the plant–pathogen interactions and plant defence responses. In this study, we reviewed the FA-mediated oxidative stress and ROS-induced defence responses of antioxidants, as well as hormonal signalling in plants. The effects of FA phytotoxicity on lipid peroxidation, physiological changes and ultrastructural changes at cellular and subcellular levels were reported. Additionally, DNA damage, cell death and adverse effects on photosynthesis have been explained. Some possible approaches to overcome the harmful effects of FA in plants were also discussed. It is concluded that FA-induced ROS affect the enzymatic and non-enzymatic antioxidant system regulated by phytohormones. The effects of FA are also associated with other photosynthetic, ultrastructural and genotoxic modifications in plants

Effects of Light and Daytime on the Regulation of Chitosan-Induced Stomatal Responses and Defence in Tomato Plants

Closure of stomata upon pathogenesis is among the earliest plant immune responses. However, our knowledge is very limited about the dependency of plant defence responses to chitosan (CHT) on external factors (e.g., time of the day, presence, or absence of light) in intact plants. CHT induced stomatal closure before dark/light transition in leaves treated at 17:00 hrs and stomata were closed at 09:00 hrs in plants treated at dawn and in the morning. CHT was able to induce generation of reactive oxygen species (ROS) in guard cells in the first part of the light phase, but significant nitric oxide production was observable only at 15:00 hrs. The actual quantum yield of PSII electron transport (ΦPSII) decreased upon CHT treatments at 09:00 hrs in guard cells but it declined only at dawn in mesophyll cells after the treatment at 17:00 hrs. Expression of Pathogenesis-related 1 (PR1) and Ethylene Response Factor 1 were already increased at dawn in the CHT-treated leaves but PR1 expression was inhibited in the dark. CHT-induced systemic response was also observed in the distal leaves of CHT-treated ones. Our results suggest a delayed and daytime-dependent defence response of tomato plants after CHT treatment at night and under darkness

Effects of Jasmonic Acid in ER Stress and Unfolded Protein Response in Tomato Plants

Endoplasmic reticulum (ER) stress elicits a protective mechanism called unfolded protein response (UPR) to maintain cellular homeostasis, which can be regulated by defence hormones. In this study, the physiological role of jasmonic acid (JA) in ER stress and UPR signalling has been investigated in intact leaves of tomato plants. Exogenous JA treatments not only induced the transcript accumulation of UPR marker gene SlBiP but also elevated transcript levels of SlIRE1 and SlbZIP60. By the application of JA signalling mutant jai1 plants, the role of JA in ER stress sensing and signalling was further investigated. Treatment with tunicamycin (Tm), the inhibitor of N-glycosylation of secreted glycoproteins, increased the transcript levels of SlBiP. Interestingly, SlIRE1a and SlIRE1b were significantly lower in jai1. In contrast, the transcript accumulation of Bax Inhibitor-1 (SlBI1) and SlbZIP60 was higher in jai1. To evaluate how a chemical chaperone modulates Tm-induced ER stress, plants were treated with sodium 4-phenylbutyrate, which also decreased the Tm-induced increase in SlBiP, SlIRE1a, and SlBI1 transcripts. In addition, it was found that changes in hydrogen peroxide content, proteasomal activity, and lipid peroxidation induced by Tm is regulated by JA, while nitric oxide was not involved in ER stress and UPR signalling in leaves of tomato