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Abscisic acid (ABA) is a stress hormone that accumulates under different abiotic and biotic stresses. A typical effect of ABA on leaves is to reduce transpirational water loss by closing stomata and parallelly defend against microbes by restricting their entry through stomatal pores. ABA can also promote the accumulation of polyamines, sphingolipids, and even proline. Stomatal closure by compounds other than ABA also helps plant defense against both abiotic and biotic stress factors. Further, ABA can interact with other hormones, such as methyl jasmonate (MJ) and salicylic acid (SA). Such cross-talk can be an additional factor in plant adaptations against environmental stresses and microbial pathogens. The present review highlights the recent progress in understanding ABA’s multifaceted role under stress conditions, particularly stomatal closure. We point out the importance of reactive oxygen species (ROS), reactive carbonyl species (RCS), nitric oxide (NO), and Ca 2+ in guard cells as key signaling components during the ABA-mediated short-term plant defense reactions. The rise in ROS, RCS, NO, and intracellular Ca 2+ triggered by ABA can promote additional events involved in long-term adaptive measures, including gene expression, accumulation of compatible solutes to protect the cell, hypersensitive response (HR), and programmed cell death (PCD). Several pathogens can counteract and try to reopen stomata. Similarly, pathogens attempt to trigger PCD of host tissue to their benefit. Yet, ABA-induced effects independent of stomatal closure can delay the pathogen spread and infection within leaves. Stomatal closure and other ABA influences can be among the early steps of defense and a crucial component of plants’ innate immunity response. Stomatal guard cells are quite sensitive to environmental stress and are considered good model systems for signal transduction studies. Further research on the ABA-induced stomatal closure mechanism can help us design strategies for plant/crop adaptations to stress.

Stomatal closure is essential to conserve water and prevent microbial entry into leaves. Alkalinization of guard cells is common during closure by factors such as abscisic acid, methyl jasmonate, and even darkness. Despite reports pointing at the role of cytosolic pH, there have been doubts about whether the guard cell pH change is a cause for stomatal closure or an associated event, as changes in membrane potential or ion flux can modulate the pH. However, the importance of cytosolic alkalinization is strongly supported by the ability of externally added weak acids to restrict stomatal closure. Using genetically encoded pH sensors has confirmed the rise in pH to precede the elevation of Ca 2+ levels. Yet some reports claim that the rise in pH follows the increase in ROS or Ca 2+ . We propose a feedback interaction among the rise in pH or ROS or Ca 2+ to explain the contrasting opinions on the positioning of pH rise. Stomatal closure and guard cell pH changes are compromised in mutants deficient in vacuolar H + -ATPase (V-ATPase), indicating the importance of V-ATPase in promoting stomatal closure. Thus, cytosolic pH change in guard cells can be related to the rise in ROS and Ca 2+ , leading to stomatal closure. We emphasize that cytosolic pH in stomatal guard cells deserves further attention and evaluation.

[...]guard cells lose turgor leading to stomatal closure (Arnaud and Hwang,2015; Agurla et al.,2018; Saito and Uozumi,2019; Hsu et al.,2021). Peroxisomal ROS could protect against plant pathogens (Sørhagen et al.,2013). Besides ROS, other components of peroxisomes, namely NO, Ca2+, and polyamines (PA), upregulated the genes involved in SA signaling and PA catabolism, reinforcing plant defense responses (Chen et al.,2016; Wang et al.,2019). The pathogens required sugars for growth and infection (Solomon et al.,2003; Scharte et al.,2005; Chang et al.,2017). [...]the deficiency in sugar availability lead to decreased fungal growth (Bezrutczyk et al.,2018). There was a positive relationship between the transpiration rate and mineral content of sunflower (Helianthus annuus) and maize leaves (Tanner and Beevers,2001; Shrestha et al.,2021). Since microbial spread and multiplication within leaves depend on macronutrients/micronutrients, the mineral deficiency could affect microbial growth and enhance pathogen tolerance (Fernández-Escobar,2019).

Stomatal guard cells are unique in that they have more mitochondria than chloroplasts. Several reports emphasized the importance of mitochondria as the major energy source during stomatal opening. We re-examined their role during stomatal closure. The marked sensitivity of stomata to both menadione (MD) and methyl viologen (MV) demonstrated that both mitochondria and chloroplasts helped to promote stomatal closure in Arabidopsis. As in the case of abscisic acid (ABA), a plant stress hormone, MD and MV induced stomatal closure at micromolar concentration. All three compounds generated superoxide and H2O2, as indicated by fluorescence probes, BES-So-AM and CM-H2DCFDA, respectively. Results from tiron (a superoxide scavenger) and catalase (an H2O2 scavenger) confirmed that both the superoxide and H2O2 were requisites for stomatal closure. Co-localization of the superoxide and H2O2 in mitochondria and chloroplasts using fluorescent probes revealed that exposure to MV initially triggered higher superoxide and H2O2 generation in mitochondria. In contrast, MD elevated superoxide/H2O2 levels in chloroplasts. However, with prolonged exposure, MD and MV induced ROS production in other organelles. We conclude that ROS production in mitochondria and chloroplasts leads to stomatal closure. We propose that stomatal guard cells can be good models for examining inter-organellar interactions.

When plants are exposed to water stress, photosynthesis is downregulated due to enhanced reactive oxygen species (ROS) and nitric oxide (NO). In contrast, photorespiratory metabolism protected photosynthesis and sustained yield. Modulation of photorespiration by ROS was established, but the effect of NO on photorespiratory metabolism was unclear. We, therefore, examined the impact of externally added NO by using S-nitrosoglutathione (GSNO), a natural NO donor, in leaf discs of pea (Pisum sativum) under dark or light: moderate or high light (HL). Maximum NO accumulation with GSNO was under high light. The presence of 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a NO scavenger, prevented the increase in NO, confirming the release of NO in leaves. The increase in S-nitrosothiols and tyrosine-nitrated proteins on exposure to GSNO confirmed the nitrosative stress in leaves. However, the changes by GSNO in the activities and transcripts of five photorespiratory enzymes: glycolate oxidase, hydroxypyruvate reductase, catalase, glycerate kinase, and phosphoglycolate phosphatase activities were marginal. The changes in photorespiratory enzymes caused by GSNO were much less than those with HL. Since GSNO caused only mild oxidative stress, we felt that the key modulator of photorespiration might be ROS, but not NO.