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Systemic acquired resistance (SAR) is a potent innate immunity system in plants that is induced through the salicylic acid (SA)-mediated signaling pathway. Here, we characterized 3-chloro-1-methyl-1H-pyrazole-5-carboxylic acid (CMPA) as an effective SAR inducer in Arabidopsis. The soil drench application of CMPA enhanced a broad range of disease resistance against the bacterial pathogen Pseudomonas syringae and fungal pathogens Colletotrichum higginsianum and Botrytis cinerea in Arabidopsis, whereas CMPA did not show antibacterial activity. Foliar spraying with CMPA induced the expression of SA-responsible genes such as PR1, PR2 and PR5. The effects of CMPA on resistance against the bacterial pathogen and the expression of PR genes were observed in the SA biosynthesis mutant, however, while they were not observed in the SA-receptor-deficient npr1 mutant. Thus, these findings indicate that CMPA induces SAR by triggering the downstream signaling of SA biosynthesis in the SA-mediated signaling pathway.

A newly identified chemical, 4-{3-[(3,5-dichloro-2-hydroxybenzylidene)amino]propyl}-4,5-dihydro-1H-pyrazol-5-one (BAPP) was characterized as a plant immunity activator. BAPP enhanced disease resistance in rice against rice blast disease and expression of a defense-related gene without growth inhibition. Moreover, BAPP was able to enhance disease resistance in dicotyledonous tomato and Arabidopsis plants against bacterial pathogen without growth inhibition, suggesting that BAPP could be a candidate as an effective plant activator. Analysis using Arabidopsis sid2-1 and npr1-2 mutants suggested that BAPP induced systemic acquired resistance (SAR) by stimulating between salicylic acid biosynthesis and NPR1, the SA receptor protein, in the SAR signaling pathway.

In recent years, it has become clear that the crosstalk of various plant hormones controls plant growth and disease resistance. Plant hormone signals may also be involved in the actions of a variety of pesticides and disease control techniques used for crop protection. From this point of view, we have focused on plant hormones to analyze the mode of action of pesticides that function in plants. Disease resistance inducers are pesticides that induce systemic acquired resistance (SAR) by activating the salicylic acid (SA)-mediated signaling pathway. However, when under unfavorable climate conditions, such as cold and cloudy weather, the resistance inducers are not sufficiently effective. Since the environmental stress response mediated by abscisic acid (ABA) may affect disease resistance, extensive studies of tobacco and tomato plants were performed, which clarified that SAR induction was suppressed by ABA. On the other hand, it was shown that transient high temperature treatment enhanced disease resistance via SA biosynthesis. These results suggest that changes in temperature due to climate change have an impact on disease resistance. The mode of action of a plant-growth regulator was analyzed by focusing on plant hormones. Isoprothiolane (IPT), an active ingredient of Fuji-one, is used as a plant-growth regulator and a fungicide. In Arabidopsis thaliana, we demonstrated that jasmonic acid and ethylene are required for the root elongation-promoting effect of IPT. As shown above, mode-of-action studies on pesticides in relation to plant hormones will lead to the development of new techniques for the better cultivation and protection of crops.

Strigolactones are low-molecular-weight phytohormones that play several roles in plants, such as regulation of shoot branching and interactions with arbuscular mycorrhizal fungi and parasitic weeds. Recently, strigolactones have been shown to be involved in plant responses to abiotic and biotic stress conditions. Herein, we analyzed the effects of strigolactones on systemic acquired resistance induced through salicylic acid-mediated signaling. We observed that the systemic acquired resistance inducer enhanced disease resistance in strigolactone-signaling and biosynthesis-deficient mutants. However, the amount of endogenous salicylic acid and the expression levels of salicylic acid-responsive genes were lower in strigolactone signaling-deficient max2 mutants than in wildtype plants. In both the wildtype and strigolactone biosynthesis-deficient mutants, the strigolactone analog GR24 enhanced disease resistance, whereas treatment with a strigolactone biosynthesis inhibitor suppressed disease resistance in the wildtype. Before inoculation of wildtype plants with pathogenic bacteria, treatment with GR24 did not induce defense-related genes; however, salicylic acid-responsive defense genes were rapidly induced after pathogenic infection. These findings suggest that strigolactones have a priming effect on Arabidopsis thaliana by inducing salicylic acid-mediated disease resistance.

Systemic acquired resistance (SAR) is a potent innate immunity system in plants and has been used in rice fields. Development of SAR, involving priming, is achieved by activation of salicylic acid (SA)-mediated pathway. To determine whether heat shock (HS) treatment can induce SAR, we analyzed the effects of HS on Arabidopsis. HS treatment induced disease resistance, expression of SAR marker genes, and SA accumulation in wild-type but not in SA-deficient sid2 and NahG plants, indicating induction of SAR. Time course analysis of the effects of HS indicated that SAR was activated transiently, differently from biological induction, with a peak at 2-3 d after HS, and that it ceased in several days. Production of reactive oxygen species was observed before SA biosynthesis, which might be a trigger for SAR activation. The data presented here suggest that HS can induce SAR, but there exist unknown regulation mechanisms for the maintenance of SAR.

Recent studies have indicated that the phytohormone abscisic acid (ABA), induced in response to a variety of environmental stresses, plays an important role in modulating diverse plant–pathogen interactions. In Arabidopsis thaliana, we previously clarified that ABA suppressed the induction of systemic acquired resistance (SAR), a plant defense system induced by pathogen infection through salicylic acid (SA) accumulation. We investigated the generality of this suppressive effect by ABA on SAR using tobacco plants. For SAR induction, we used 1,2-benzisothiazole-3(2H)-one 1,1-dioxide (BIT) and benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH) that activate upstream and downstream of SA in the SAR signaling pathway, respectively. Wild-type tobacco plants treated with BIT or BTH exhibited enhanced disease resistance against Tobacco mosaic virus (TMV) and tobacco wildfire bacterium, Pseudomonas syringae pv. tabaci (Pst), however, which was suppressed by pretreatment of plants with ABA. Pretreatment with ABA also suppressed the expression of SAR-marker genes by BIT and BTH, indicating that ABA suppressed the induction of SAR. ABA suppressed BTH-induced disease resistance and pathogenesis-related (PR) gene expression in NahG-transgenic plants that are unable to accumulate SA. The accumulation of SA in wild-type plants after BIT treatment was also suppressed by pretreatment with ABA. These data suggest that ABA suppresses both upstream and downstream of SA in the SAR signaling pathway in tobacco.