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Figure 1. 

A simplified overview of how plants perceive and respond to salinity. In the left panel, orange arrows indicate the process by which salt stress induces osmotic, ionic, and oxidative stress and affects the normal functioning of plants, while green arrows represent the perception, signal transduction, and adaptive responses of plants to salinity. The right panel details three key aspects: (a) the negative impacts of salt stress on plant growth and development; (b) the signal transduction pathway activated by salt stress. In the figure, GIPC refers to the sodium ion receptor glycosyl inositol phosphorylceramide; (c) multiple regulatory mechanisms operating at the transcriptional and protein levels to facilitate adaptive responses. This figure was created using https://BioRender.com.

Figure 2. 

A simplified overview of JA signaling transduction in plants. In the resting state, JAZ recruits a transcriptional repressor complex (JAZ–NINJA–TPL) to inhibit the activity of core transcription factors (e.g., MYC2). When plants sense specific developmental signals or experience stress conditions, the bioactive JA-Ile level increases. Upon binding to COI1, JA-Ile promotes the degradation of JAZ proteins via the 26S proteasome pathway, thereby activating the expression of downstream response genes. This process involves multiple proteins. For example, the key transcription factor MYC2 directly interacts with the Mediator subunit MED25 and recruits Pol II to initiate transcription. As indicated by the pink arrows, MYC2 acts as a key integrator that mediates crosstalk among multiple signaling pathways, including various phytohormone signaling pathways. The JA signaling pathway regulates diverse aspects of plant growth and development, as well as responses to both biotic and abiotic stresses. The seven colored boxes at the bottom of the figure represent processes regulated by JA signaling. '26S' is the abbreviation of the 26S proteasome degradation pathway. This figure was created using https://BioRender.com.

Figure 3. 

Mechanisms of salt stress-induced JA biosynthesis in plants. Salt stress induces JA biosynthesis through multiple pathways, with ethylene, ABA, ROS, and polyamines acting as upstream regulators. Blue text marks known triggers/events that promote JA biosynthesis under salt stress. Among them, the membrane receptor FER inhibits the accumulation of the active form of ABA, but under salt stress, the RALF–LRX–S1P module triggers FER internalization. The accumulation of JA under salt stress is primarily achieved by upregulating the expression of enzymes involved in JA biosynthesis. Several transcription factors have been reported to directly participate in this process. Solid arrows indicate direct regulatory relationships between transcription factors and their target genes that are supported by evidence, while IbGATA24 is involved in this process but lacks identified direct target genes. Enzymes are presented in the order of the JA biosynthetic pathway to show the regulatory points of transcription factors. Dashed lines in the figure indicate a causal relationship that is not direct or lacks more concrete evidence, while solid lines represent well-established and more direct regulatory interactions. This figure was created using https://BioRender.com.

Figure 4. 

Mechanisms of JA signaling in plant adaptation to salt stress. Salt stress induces JA signaling, which subsequently enhances plant salt tolerance. According to current reports, such tolerance mainly centers on responding to ionic and oxidative stress. The left panel shows JA-mediated regulation of ion homeostasis under salt stress, with red text indicating the species in which each pathway has been reported. Under salt stress, JA mainly regulates ion homeostasis by activating key transcriptional regulators (e.g., SlWRKY80/81), which in turn modulate the expression or activity of ion channels and proton pumps. JA signaling promotes the expression of the vacuolar membrane Na⁺/H⁺ antiporter NHX, enhances proton pump activity, and increases ATP accumulation, indirectly enabling the proton pump to provide more H⁺ ions required by NHX. The right panel shows the mechanisms by which JA regulates the antioxidant system under salt stress, mainly through upregulating the expression of antioxidant enzyme genes (POD, CAT, APX, SOD) and promoting the accumulation of antioxidant compounds (carotenoids, anthocyanin, chlorophyll b, GSH) to scavenge ROS. Dashed lines in the figure indicate a causal relationship that is not direct or lacks more concrete evidence, while solid lines represent well-established and more direct regulatory interactions. This figure was created using https://BioRender.com.

Figure 5. 

Signal pathways and components involved in JA-mediated regulation of seed germination inhibition and root growth inhibition. Under moderate salt stress, JA reshapes root architecture and suppresses seed germination. Purple arrows indicate the core process of the JA-mediated salt stress response under moderate salt stress: salt stress induces JA-Ile accumulation, which further activates gene expression through degradation of JAZ proteins (JAZ1/2/5/7/8/9/11/12). JAZs inhibit the function of MYC2/3/4, but promote RSS3 to suppress the function of OsbHLH089/094. This leads to the suppression of genes regulating cell division and growth, such as CycB2;1 and PLTs, thereby inhibiting root growth. At the same time, MYC2 also suppresses the expression of P5CS1 (encodes a key enzyme in proline synthesis) and CAT2 (encodes a key enzyme in ROS scavenging). These events reduce proline accumulation and maintain ROS levels for signaling. Consequently, seed germination is inhibited, and root architecture is altered. In addition, salt stress also affects this main pathway through other signaling routes. For example, it activates the MPK cascade MKK3–MPK6, which phosphorylates MYC2 and enhances its function. Salt stress also promotes the expression of JAZ5/7/8, CkMYC2, and CkPYL4 (encodes ABA receptor CkPYL4) through mechanisms that are not yet fully understood. CkPYL4 inhibits the ABA signaling repressor CkPP2C and the key ABA metabolism enzyme CkCYP70A4, leading to ABA accumulation, which further promotes the accumulation of JA-Ile. Under salt stress, CYP94C2b catalyzes the conversion of the active form JA-Ile into the storage forms 12OH-JA-Ile/12COOH-JA-Ile, preventing overactivation of the signaling pathway. Dashed lines in the figure indicate a causal relationship that is not direct or lacks more concrete evidence, while solid lines represent well-established and more direct regulatory interactions. '26S' is the abbreviation of the 26S proteasome degradation pathway. This figure was created using https://BioRender.com.

Figure 6. 

Mechanisms of JA-mediated stomatal development and photosynthetic acclimation under salt stress. Under moderate salt stress, CO₂ uptake and photosynthesis are limited. JA plays a dual role in this adaptive response: purple arrows indicate the core process of JA-mediated shoot physiological responses under salt stress. Salt stress induces JA accumulation, which further activates JA signaling by degrading JAZ proteins. JA signaling promotes the expression of CkMYC2 and CkPYL4. CkMYC2 and CkPYL4 facilitate the formation of the CkPP2C–CkMYC2–CkPYL4 complex. This complex inhibits the key ABA metabolism enzyme CkCYP70A4, leading to ABA accumulation. Elevated ABA levels then suppress stomatal development, reduce stomatal density, and consequently limit CO₂ uptake and transpiration. Concurrently, JA enhances photosynthetic efficiency by upregulating Rubisco activase A (RcaA), illustrating a sophisticated balance between stress adaptation and growth maintenance. RcaA mediates the activation of Rubisco, the core enzyme responsible for CO₂ fixation in photosynthesis, thereby facilitating efficient carbon assimilation. Dashed lines in the figure indicate a causal relationship that is not direct or lacks more concrete evidence, while solid lines represent well-established and more direct regulatory interactions. '26S' is the abbreviation for the 26S proteasome degradation pathway. A glow effect is added to elements to indicate JA-mediated activation of protein activity. This figure was created using https://BioRender.com.

Figure 7. 

Mechanisms of JA signaling in modulating plant survival under severe salinity. Under severe salinity stress, plants face a survival threat. Excessive ion accumulation and ROS production are major causes of plant death. JA promotes survival by countering ion toxicity and oxidative damage, primarily through transcriptional regulation involving the degradation pathway of JAZ proteins (JAZ8, SlJAZ1) and other poorly understood mechanisms (dashed lines from JA-Ile). On the left of this figure, JA forms a positive feedback loop with spermidine (Spd) to amplify signaling. JA signaling achieves this process by regulating the expression of the key Spd synthase SlSPDS2, which is controlled by the transcription factors MYC2 and SlWRKY42/80. SlWRKY80 is repressed by SlJAZ1; however, under salt stress, JA signaling suppresses SlJAZ1 expression and promotes SlJAZ1 degradation. On the right, JA activates JAZ8 degradation to regulate antioxidant defense and ion homeostasis, achieving multilayer regulation of anthocyanin accumulation. Degradation of JAZ8 relieves its repression on the NF-Y complex (NF-YB2–NF-YA1–NF-YC9), promoting the expression of MYB75. This facilitates the formation of the WD-repeat/bHLH/MYB complex (WD40–TT8–MYB75). Additionally, the degradation of JAZ8 also relieves the suppression of the JAZ–ECAP–TPR2 repressor complex on the WD-repeat/bHLH/MYB complex. These events collectively enhance the activation of transcription of anthocyanin biosynthesis genes by the WD-repeat/bHLH/MYB complex. '26S' denotes the 26S proteasome degradation pathway. This figure was created using https://BioRender.com.