Jasmonic acid upregulation enhances tomato tolerance to concurrent high light and heat stress

Plants are constantly challenged by environmental stresses that significantly affect their growth and development. In the field, high light (HL) and heat stress (HS) are common and concurrently occur during hot summer days. Each stress on its own decreases photosynthesis and plant health, but when they coincide, the damage is more severe than either stress alone. HL impacts photosynthetic machinery, while HS inhibits the repair mechanism of photosystems. Combined stress triggers production of distinct reactive oxygen species (ROS), which leads to activation of specific adaptive and signaling responses in plants (Yadav et al. 2020; Zeng et al. 2024).

Tomato (Solanum lycopersicum L.) is an economically important crop and grows optimally at temperatures between 25 °C and 30 °C, so it is often negatively affected by HL and HS (Zhou et al. 2020). Understanding how tomato plants adapt to such stress combinations is essential for breeding more resilient varieties. Recent work has indicated that plants adapt to HS and HL stress by increasing endogenous jasmonic acid (JA), which is a key regulator in defense and developmental processes (Huang et al. 2023). However, the mechanism by which JA helps plants deal with combined HL + HS remained unclear.

To investigate the role of JA signaling, He et al. (2025) analyzed wild-type tomato plants (Castlemart, CM) and the jasmonic acid–insensitive1–1 (jai1-1) mutant under high light (HL, 1200 μmol m⁻² s⁻¹), high temperature (HS, 42 °C), and combined stress, while controls were maintained at 300 μmol m⁻² s⁻¹ and 25 °C throughout the experiment. Under control conditions, both genotypes exhibited similar phenotypes. HS treatment caused minor visible damage, and HL produced mild chlorosis in the jai1-1 mutant. The combined HL + HS displayed severe chlorosis and extensive tissue damage in the jai1-1 mutant, while wild-type plants remained largely intact. Leaf Damage Index quantification confirmed that jai1-1 mutant leaves were severely affected compared with wild type. These results demonstrated that JA signaling is crucial for tomato tolerance to HL + HS (Fig. A).

Figure.

JA mediates tolerance in tomato under HL and HS. A) Representative images from (He et al. 2025) of 4-week-old wild-type (Castlemart, CM), jai1-1 (jasmonate-insensitive1-1), SlST2A transgenic lines, and SlHSFB2b transgenic lines subjected to control and combined HL + HS treatments. The red and orange arrows indicate severely and minor photobleached leaves, respectively. Relative JA levels are shown in high and low pink boxes. White bar represents 2 cm per scale. B) Schematic illustration showing that HL and HS together induce SlHSFB2b, which represses SlST2A that converts typically JA to its inactive sulfated form. The suppression of SlST2A increases JA levels, activating the SlMYC2 signaling pathway. SlMYC2 upregulates transcription factors and various functional genes that protect photosystem II and detoxify ROS. Illustration recreated using Biorender.

To understand the molecular basis of JA signaling under HL + HS, He et al. (2025) performed a transcriptome analysis. RNA-seq analysis of WT and jai1-1 under HS, HL, and HL + HS revealed differential expression of multiple JA biosynthetic and metabolic genes. Among them, sulfotransferase-encoding genes (Solyc05g011890, SlST2A), which convert active JA into inactive 12-hydroxy-JA (12OH-JA) through sulfation (Hirschmann et al. 2014), exhibited the most significant downregulation under HL + HS. The authors hypothesized that tomato may regulate the pool of bioactive JAs under HL + HS stress via SlST2A-mediated sulfation, which was confirmed by generating Sist2a mutants and overexpressing (OE) lines. Mutant and OE line analyses confirmed this relationship. Slst2a mutants accumulated significantly higher JA and bioactive jasmonoyl-(L)-isoleucine (JA-Ile), and only trace amounts of 12OH-JA and Slst2a mutant lines were more tolerant to stress. In comparison, SlST2A OE lines showed reduced JA levels, elevated 12OH-JA levels, greater leaf damage, and reduced PSII efficiency than control.

Next, RNA-seq analysis was conducted to identify the upstream regulators of SlST2A. He et al. (2025) observed that the heat shock factor B (HSFB) family transcription factor SlHSFB2b showed a significant upregulation under HL + HS compared with control. Members of the HSF family are central to plant responses to heat and other abiotic stresses, mediating both rapid transcriptional activation and epigenetic stress memory (Jacob et al. 2017). To validate its function, SlHSFB2b knockout and OE lines were generated using CRISPR/Cas9 and transgenic approaches. Under HL + HS, SlHSFB2b overexpression increased JA and JA-Ile content, while the knockouts accumulated less. DNA-binding assays (yeast 1-hybrid and dual-luciferase tests) also showed that SlHSFB2b binds directly to the SlST2A promoter and suppresses its expression. Physiological measurements confirmed that SlHSFB2b overexpression improved PSII efficiency and reduced leaf damage, whereas the mutants were more sensitive. These results demonstrate that SlHSFB2b acts as a transcriptional repressor of SlST2A, reducing JA catabolism and thereby elevating endogenous JA levels under HL + HS.

Further, it was observed that increased JA levels under HL + HS activate MYC2-regulated transcriptional cascades that coordinate with other regulators to enhance tolerance to HL + HS by reinforcing PSII protection. Interestingly, authors also investigated that SlHSFB2b itself appears to be regulated by SlMYC2, suggesting a positive feedback loop that maintains JA signaling during prolonged stress. Weighted gene coexpression network analysis of wild-type and jai1-1 plants was conducted to understand the genes and pathways that contribute to tomato tolerance to combined stress. The authors identified a group of genes related to responses to heat, ROS, and high light that were highly expressed in control but not in jai1-1 under HL + HS, suggesting that JA signaling is required for their activation (Fig. B).

This study describes how tomato plants adapt to simultaneous HL and HS. Instead of increasing JA production, the plants save energy by limiting its breakdown. By repressing SlST2A, SlHSFB2b prevents JA sulfation and maintains more of the hormone in its active form. This is an interesting energy-efficient strategy, allowing the plant to sustain its defense without a large metabolic cost. From an applied perspective, the SlHSFB2b–SlST2A module is a promising target for crop improvement. Engineering these genes could enhance stress tolerance without incurring significant growth penalties as both mutants and OE grew normally under control conditions.

Data availability

No new data included in this article.