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Plant activators have emerged as promising alternatives to conventional crop protection chemicals for managing crop diseases due to their unique mode of action. By priming the plant's innate immune system, these compounds can induce disease resistance against a broad spectrum of pathogens without directly inhibiting their proliferation. Key advantages of plant activators include prolonged defense activity, lower effective dosages, and negligible risk of pathogen resistance development. Among the various defensive pathways targeted, the salicylic acid (SA) signaling cascade has been extensively explored, leading to the successful development of commercial activators of systemic acquired resistance, such as benzothiadiazole, for widespread application in crop protection. While the action sites of many SA-targeting activators have been preliminarily mapped to different steps along the pathway, a comprehensive understanding of their precise mechanisms remains elusive. This review provides a historical perspective on plant activator development and outlines diverse screening strategies employed, from whole-plant bioassays to molecular and transgenic approaches. We elaborate on the various components, biological significance, and regulatory circuits governing the SA pathway while critically examining the structural features, bioactivities, and proposed modes of action of classical activators such as benzothiadiazole derivatives, salicylic acid analogs, and other small molecules. Insights from field trials assessing the practical applicability of such activators are also discussed. Furthermore, we highlight the current status, challenges, and future prospects in the realm of SA-targeting activator development globally, with a focus on recent endeavors in China. Collectively, this comprehensive review aims to describe existing knowledge and provide a roadmap for future research toward developing more potent plant activators that enhance crop health. [ABSTRACT FROM AUTHOR]

Xanthomonas campestris pv. campestris (Xcc) is a significant phytopathogen causing black rot disease in crucifers. Its virulence relies heavily on the type III secretion system (T3SS), facilitating effector translocation into plant cells. The type III effectors (T3Es) disrupt cellular processes, promoting pathogen proliferation. However, only a few T3Es from Xcc have been thoroughly characterized. In this study, we further investigated two effectors using the T3Es-deficient mutant and the Arabidopsis protoplast system. XopE2Xcc triggers Arabidopsis immune responses via an unidentified activator of the salicylic acid (SA) signaling pathway, whereas XopLXcc suppresses the expression of genes associated with patterns-triggered immunity (PTI) and the SA signaling pathway. These two effectors exert opposing effects on Arabidopsis immune responses. Additionally, we examined the relationship between the specific domains and functions of these two effector proteins. Our findings demonstrate that the N-myristoylation motif and N-terminal domain are essential for the subcellular localization and virulence of XopE2Xcc and XopLXcc, respectively. These novel insights enhance our understanding of the pathogenic mechanisms of T3Es and contribute to developing effective strategies for controlling bacterial disease. [ABSTRACT FROM AUTHOR]

Botrytis cinerea is a common pathogenic agent, causing a significant reduction in tomato quality and yield. In this study, the potential of two biocontrol fungal agents, Trichoderma harzianum and Clonostachys rosea to prevent and alleviate B. cinerea infection was assessed. To this end, the fungicidal effects of both biocontrol fungi were evaluated on ten common phytopathogens, including B. cinerea. Then, various ratios of T. harzianum and C. rosea mixtures were assessed to find the ratio that best promotes the growth of tomato seedlings and prevents the establishment of B. cinerea. The results showed that T. harzianum and C. rosea had significant fungicidal effects on all tested phytopathogens. Also, both biocontrol agents reduced the establishment of B. cinerea, in vitro assays, indicating they had significant fungicidal effects against this phytopathogen. However, when applied as a biofungicide to tomato plants, a combination of both biocontrol agents gave better control of B. cinerea. Investigating the molecular basis of resistance to B. cinerea induced by the mixture of T. harzianum and C. rosea revealed that the salicylic acid signaling pathway plays an important role in modulating the antioxidant enzyme activity. Taken together, the results of this research confirmed that both biocontrol fungal agents could induce the mechanism of B. cinerea resistance in tomato plants and shed light on the regulatory pathways associated with the resistance mechanism. [ABSTRACT FROM AUTHOR]

Xanthomonas campestris pv. campestris (Xcc) is a significant phytopathogen causing black rot disease in crucifers. Its virulence relies heavily on the type III secretion system (T3SS), facilitating effector translocation into plant cells. The type III effectors (T3Es) disrupt cellular processes, promoting pathogen proliferation. However, only a few T3Es from Xcc have been thoroughly characterized. In this study, we further investigated two effectors using the T3Es-deficient mutant and the Arabidopsis protoplast system. XopE2Xcc triggers Arabidopsis immune responses via an unidentified activator of the salicylic acid (SA) signaling pathway, whereas XopLXcc suppresses the expression of genes associated with patterns-triggered immunity (PTI) and the SA signaling pathway. These two effectors exert opposing effects on Arabidopsis immune responses. Additionally, we examined the relationship between the specific domains and functions of these two effector proteins. Our findings demonstrate that the N-myristoylation motif and N-terminal domain are essential for the subcellular localization and virulence of XopE2Xcc and XopLXcc, respectively. These novel insights enhance our understanding of the pathogenic mechanisms of T3Es and contribute to developing effective strategies for controlling bacterial disease.

Inositol pyrophosphates (PP-InsPs), derivatives of inositol hexakisphosphate (phytic acid, InsP6) or lower inositol polyphosphates, are energy-rich signaling molecules that have critical regulatory functions in eukaryotes. In plants, the biosynthesis and the cellular targets of these messengers are not fully understood. This is because, in part, plants do not possess canonical InsP6 kinases and are able to synthesize PP-InsP isomers that appear to be absent in yeast or mammalian cells. This review will shed light on recent discoveries in the biosynthesis of these enigmatic messengers and on how they regulate important physiological processes in response to abiotic and biotic stresses in plants. [ABSTRACT FROM AUTHOR]

Inositol pyrophosphates (PP-InsPs), derivatives of inositol hexakisphosphate (phytic acid, InsP6) or lower inositol polyphosphates, are energy-rich signaling molecules that have critical regulatory functions in eukaryotes. In plants, the biosynthesis and the cellular targets of these messengers are not fully understood. This is because, in part, plants do not possess canonical InsP6 kinases and are able to synthesize PP-InsP isomers that appear to be absent in yeast or mammalian cells. This review will shed light on recent discoveries in the biosynthesis of these enigmatic messengers and on how they regulate important physiological processes in response to abiotic and biotic stresses in plants.

Plant viruses cause a range of plant diseases symptoms that are often responsible for significant crop production losses and the severity and spread of the symptoms may be affected by climate change. While the increase in anthropogenic activities has caused a critical problem of increased CO2 levels in the atmosphere, these elevated CO2 levels have been reported to reduce virus disease severity in some plant species. In such instances, it is not clear if the plant defense mechanisms are being enhanced or virus-mediated mechanisms to overcome plant resistance are being defeated. Additionally, a few studies have been attempted in this area to determine if reduced disease is the norm or the exception under enhanced CO2 levels. In the present study, the effects of elevated CO2 levels (750 ppm vs. 390 ppm) on RNAi-mediated resistance of Nicotiana tabacum against the cucumber mosaic virus (CMV), and the activity of viral suppressor of RNAi (VSR) 2b protein of CMV were evaluated. On the one hand, our results showed that elevated CO2 decreased the transcription of dicer-like protein 2 (DCL2), DCL4, and argonaut 1 (AGO1) genes with functions related to RNAi-mediated resistance when infected by CMV, which is contradictory with the decreased CMV copy numbers under elevated CO2. On the other hand, we found that elevated CO2 increased the calcium concentration and expression of the calcium-binding protein rgs-CaM in tobacco plants when infected by CMV, which directly weakened the function of 2b protein, the VSR of CMV, and therefore decreased the infection efficiency of the virus and suppressed the severity of CMV in tobacco plants under elevated CO2. This study provides molecular insights into the ecological implications underlying the development of prevention strategies against plant virus infection in the context of climate change.

The objective of this study was to investigate the effect of chlorogenic acid (CGA) treatment on induction of resistance against pathogens in peach fruit. Treatment with CGA at 25–150 mg L −1 was effective at reducing lesion diameter and decay index of peach fruit during storage at 25 °C after Penicillium expansum infection. CGA treatment had also significant beneficial effects on fruit quality parameters including firmness, soluble solids contents, pH value, and titratable acidity. Activities of main defense-related enzymes and expression of key genes involved in the salicylic acid (SA) signaling pathway, such as PAL , ICS , WRKY , NPR1 , PR1 , CHI , GLU , PR5 , and POD , were enhanced by CGA treatment. These findings suggest that CGA treatment is a promising approach to controlling postharvest blue mold rot in peach fruit, and activation of the SA signaling pathway may play a potential role in mechanisms involving CGA-induced plant disease resistance. [ABSTRACT FROM AUTHOR]

Aims: Phytophthora root and stem rot caused by the oomycete plant pathogen Phytophthora sojae (Kaufmann & Gerdemann) , is a destructive disease of soybean [ Glycine max (L.) Merr.]. There is no straightforward available method to control this disease. The present study aimed to isolate a biocontrol agent (BCA) to control Phytophthora rot and gain insights into the mechanisms of biocontrol activity. Methods: Antagonistic bacteria screening, inoculation assays, histochemical and fluorometric staining and real-time polymerase chain reaction (RT-PCR) were used to achieve the goals of the present study. Results: The results indicated that the isolated BCA strain JSCX-1 was characterized as Bacillus altitudinis. Further studies showed that JSCX-1 bacterial filtrate inhibited the mycelial growth and zoospore germination of P. sojae. Greenhouse experiments showed that biocontrol efficiency of JSCX-1 against P. sojae was 49.28 ± 3.42%. Our results revealed that JSCX-1 increased the reactive oxygen species (ROS) production and callose deposition of soybean leaves. Moreover, JSCX-1 up-regulated the transcriptional level of the G. max PR1a gene but not that of the LOX and ERF genes. Conclusions: B. altitudinis JSCX-1 can effectively reduce the infectivity of P. sojae via increasing the ROS production and callose deposition on soybean, and up-regulating the expression of salicylate-responsive gene GmPR1a. [ABSTRACT FROM AUTHOR]

Vanisulfane is a plant resistance inducer that exhibits potent activity against potato virus Y (PVY), but its mechanism of action against this virus remains unclear. Our results showed that when we used 400 μg/mL of vanisulfane, it provided an impressive level of control (63.55%) against PVY in Nicotiana benthamiana L. Meanwhile, vanisulfane increased activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), and phenylalanine ammonia lyase (PAL) as well as inducing H 2 O 2 accumulation and Ca 2+ influx to mediate PVY resistance. Furthermore, combined transcriptome and proteome analyses revealed that vanisulfane upregulated the POD52, APX, and PR-1 genes and proteins in the salicylic acid (SA) signaling pathway. Experiments demonstrated that vanisulfane triggered the accumulation of SA, upregulated the expression of ICS1 and PR-1 genes, and induced resistance against PVY in transgenic Arabidopsis plants. Consequently, it can be concluded that vanisulfane mediates the SA-dependent signaling pathway to confer PVY resistance in plants.

(E)-2-Hexenal is one of the most prevalent and abundant volatile substances in fruits. Many researchers have attempted fumigation with (E)-2-hexenal to control fungal diseases with poor or no results; the key is the inability to maintain an effective concentration for a long time. Therefore, a new starch-based antifungal coating with (E)-2-hexenal microcapsules was prepared. The obtained results showed that the microcapsule embedding rate reached 78.95% by orthogonal optimization experiments and that the (E)-2-hexenal-based coating was effective at reducing the lesion diameter of apple fruit during storage at 25 °C after Penicillium expansum infection, and in other fruits; it also achieved a good antifungal effect. Moreover, the activities of the main defense-related enzymes and the expression of key genes involved in the salicylic acid (SA) signaling pathway, such as CHI, GLU, PAL , NPR1 , and PR1 , were enhanced by (E)-2-hexenal-based coating treatment. These findings suggest that the (E)-2-hexenal-based coating has the dual effect of direct antifungal and induction of apple system resistance. E2H-based coating is a promising approach to control postharvest Penicillium expansum in fruit. • E2H-based coating effectively inhibiting the growth of Penicillium expansum in apple. • E2H-based coating antifungal effect is widespread in fruits. • E2H-based coating initiates the SA signaling pathway. • E2H-based coating induces an increase in the resistance-related genes and enzymes in apple. [ABSTRACT FROM AUTHOR]

Verticillium wilt (VW) is caused by Verticillium dahliae and significantly impacts cotton yield and quality. Breeding of resistant varieties is the most effective strategy for controlling VW. Therefore, it is important to identify VW resistance genes. The diploid wild cotton species Gossypium australe is highly resistant to VW. This study identified 33 CC-NBS-LRR (CNL) genes in the G. australe genome. GauCNL expression pattern (EP) analyses showed that EP1 cluster which included four of the 33 genes, were significantly up-regulated after V. dahliae inoculation. The EP1 cluster genes were then introduced into Arabidopsis thaliana wild type Col-0, respectively. The results showed GauCNL18 overexpression significantly increased V. dahliae resistance, indicating the functional importance of GauCNL18. GauCNL18 promotes V. dahliae resistance by activating the salicylic acid signaling pathway to mediate up-regulating pathogenesis-related genes and reactive oxygen species accumulation. This study identified a CNL resistance gene, GauCNL18 , and revealed its resistance mechanism to V. dahliae. • Verticillium wilt is caused by Verticillium dahliae and significantly impacts cotton yield and quality. • The diploid wild cotton species Gossypium australe is highly resistant to Verticillium wilt. • GauCNL18 overexpression significantly increased Verticillium dahliae resistance in Arabidopsis thaliana. • GauCNL18 promotes Verticillium dahliae resistance by activating the salicylic acid signaling pathway to mediate up-regulated pathogenesis-related genes and reactive oxygen species accumulation. [ABSTRACT FROM AUTHOR]

Plant viruses cause a range of plant diseases symptoms that are often responsible for significant crop production losses and the severity and spread of the symptoms may be affected by climate change. While the increase in anthropogenic activities has caused a critical problem of increased CO2 levels in the atmosphere, these elevated CO2 levels have been reported to reduce virus disease severity in some plant species. In such instances, it is not clear if the plant defense mechanisms are being enhanced or virus-mediated mechanisms to overcome plant resistance are being defeated. Additionally, a few studies have been attempted in this area to determine if reduced disease is the norm or the exception under enhanced CO2 levels. In the present study, the effects of elevated CO2 levels (750 ppm vs. 390 ppm) on RNAi-mediated resistance of Nicotiana tabacum against the cucumber mosaic virus (CMV), and the activity of viral suppressor of RNAi (VSR) 2b protein of CMV were evaluated. On the one hand, our results showed that elevated CO2 decreased the transcription of dicer-like protein 2 (DCL2), DCL4, and argonaut 1 (AGO1) genes with functions related to RNAi-mediated resistance when infected by CMV, which is contradictory with the decreased CMV copy numbers under elevated CO2. On the other hand, we found that elevated CO2 increased the calcium concentration and expression of the calcium-binding protein rgs-CaM in tobacco plants when infected by CMV, which directly weakened the function of 2b protein, the VSR of CMV, and therefore decreased the infection efficiency of the virus and suppressed the severity of CMV in tobacco plants under elevated CO2. This study provides molecular insights into the ecological implications underlying the development of prevention strategies against plant virus infection in the context of climate change. [ABSTRACT FROM AUTHOR]