Biological Science: Research Developments and Innovations Vol. 3

Climate warming increasingly exposes plants to heat episodes while they are simultaneously challenged by pathogens and herbivores. These combinations cannot be understood as the arithmetic addition of heat and biotic stress because both perturb the same signalling infrastructure, particularly phytohormone networks and reactive oxygen species (ROS). This critical narrative review evaluates how these networks are rewired during combined heat and biotic stress, with emphasis on salicylic acid (SA), jasmonate (JA), abscisic acid (ABA), ethylene, growth-related hormones, respiratory burst oxidase homologues, calcium-dependent signalling, redox control, and temperature-sensitive immune transcriptional modules. Literature published from 2000 to 4 July 2026 was considered, with earlier seminal studies retained where mechanistically necessary. The evidence is strongest for temperature-sensitive SA immunity in Arabidopsis, where warm conditions can suppress defence-associated GBPL3 condensate formation and the CBP60g–SARD1 transcriptional module, reducing local SA production and systemic N-hydroxypipecolic acid-dependent acquired resistance. ROS emerge not as a single oxidative variable but as compartment-, amplitude-, and time-dependent signals that connect pattern recognition, intracellular immune receptors, stomatal behaviour, thermotolerance and systemic acclimation. JA and ABA illustrate consequential trade-offs: signalling that protects against herbivory or water loss can compromise transpirational cooling or temperature-sensitive resistance, depending on context. Evidence from tomato, apple and other crops also shows that warming can enhance, suppress or qualitatively redirect defence according to thermal regime, tissue exposed, attacker lifestyle, host genotype and pathogen thermophysiology. The central limitation of the field is therefore not lack of candidate components, but inadequate resolution of their spatiotemporal interactions under realistic stress sequences. Future progress requires factorial heat–biotic experiments, cell-resolved redox and hormone measurements, simultaneous host–attacker phenotyping and conditional engineering of integrator nodes rather than constitutive activation of defence.