Molecular Pathogens, 2025, Vol.16, No.4, 193-206 http://microbescipublisher.com/index.php/mp 196 plants that overexpress positive regulators of JA signal show stronger resistance to disease when faced with infection with grey mold bacteria (necrotic pathogen). In addition, the synergy between JA and ethylene can induce cucumbers to produce volatiles and plant protection enzymes, and fight against virus-borne vector insects such as aphids, thereby indirectly reducing the virus transmission rate. 3.3 The dual role of ethylene (ET) in defense signals Ethylene (ET) is a simple gas hormone that plays a role in both plant growth and development and stress responses. Especially in plant immunity, ethylene signals can be positively regulated or negatively regulated certain defensive responses, which is called "dual role". On the one hand, ET often cooperates with the JA pathway to fight stresses such as necrotic pathogens and insect feeding. The study found that in a variety of plants such as cucumber, the co-activation of JA and ET signals can significantly enhance resistance to necrotic diseases such as grey mold and root rot (Wu et al., 2025). ET can induce the expression of a series of defense genes, such as callose synthesis-related genes, CHI (chitinase), etc., improve cell wall toughness, decompose pathogenic cell walls, and limit pathogen invasion. At the same time, ET can also promote the production of volatile substances in plants to attract pathogens to antagonize microorganisms or natural enemies, and help plants resist diseases and insects at the ecological level. In addition, ET is involved in regulating the aging procedures of plants, and moderate tissue necrosis helps to form a "brown fence" that limits pathogen expansion. On the other hand, in certain biological pathogen infestations, premature or excessive activation of ET signals may lead to adverse effects on the host. Many biotrophic bacteria (such as Xanthomonas) induce ethylene synthesis in host plants, triggering premature aging and tissue softening, thereby improving bacterial nutrient acquisition and pathogenicity. This suggests that ethylene promotes pathogenic infection in specific situations, showing a negative regulatory role. In the cucumber-downer fungi interaction, it has been observed that sensory varieties produce higher levels of ethylene in the early stages of infection, accompanied by rapid yellowing and necrosis of leaves, while disease-resistant varieties have weak ethylene response and controlled cell death, thus limiting pathogen expansion (Yang et al., 2025). This phenomenon shows that ethylene-induced allergic cell death may do more harm than good in some chronic diseases, giving the pathogen a chance. In addition, there is an antagonistic relationship between ethylene and SA signal. High levels of ethylene sometimes inhibit SA-dependent system resistance, making plants more susceptible to biological pathogens. 4 Interaction Between Hormones and Signaling Network Integration 4.1 SA-JA antagonism and synergistic effects Plant hormone signals do not play an independent role, but achieve fine regulation of immune responses through complex network interactions. Among them, the two main resistance signaling pathways, SA and JA, usually show an antagonistic relationship: when one pathway is activated, the effect of the other pathway is often inhibited. This antagonism is considered a trade-off for plants to fight biological and necrotic pathogens under limited resources. Specifically, SA-mediated immunity is most effective against biotrophic pathogens (such as Downy and Powdery) while JA-mediated immunity is more suitable for the treatment of necrotic trophic pathogens and plant-eating insects. When plants feel the signal of pathogen infestation, the corresponding pathway is activated according to the type of pathogen and avoids "error" responses by inhibiting another pathway. For example, when cucumbers are infected with downy mildew, SA levels rise rapidly and induce SAR responses, while JA signal is downregulated to concentrate resources on SA-dependent defense (Luan et al., 2019). This SA-JA antagonism can be explained from the molecular level: after SA accumulation, it can induce the expression of the transcription factor WRKY70, which is both a positive regulator of SA signal and a key gene in the JA signaling pathway, thereby achieving suppression of JA response at the gene expression level. Correspondingly, activated transcription factors (such as ERFs) of the JA pathway can also indirectly attenuate gene expression of the SA pathway. Furthermore, some co-regulatory elements (such as NPR1) interact with negative regulators of JA signal at high concentrations of SA, resulting in the inhibition of JA response genes (Caarls et al., 2015; Chen et al., 2019).
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