Heat, cold and drought challenge plant immunity in the face of climate change

Rising global temperatures, accompanied by extreme events such as droughts, floods, and heat waves, threaten agriculture and food security. Plants, which cannot move, rely exclusively on innate immunity to defend themselves against microorganisms. This defense involves cell surface sensors and intracellular proteins that recognize signs of invasion.

Recent research shows that environmental changes affect the expression of genes linked to these sensors. Temperature, water deficit, and cold directly modulate pattern receptors (PRRs) and cell wall integrity (CWI) sensors, crucial components of plant immunity. This is the finding of scientists from the Free University of Brussels (ULB) and the University of Paris-Saclay.

Danger sensors and immune response

Plants recognize pathogens through two main mechanisms: pattern-triggered immunity (PTI) and damage-triggered immunity (DTI). Both rely on the activation of PRRs, proteins located in the cell membrane that detect microbial fragments or signs of damage.

In more severe cases, intracellular proteins called NLRs recognize pathogen-specific molecules, initiating so-called effector-triggered immunity (ETI).

These systems work in an integrated manner. PTI and DTI block the initial advance of the pathogen, while ETI kicks in when these barriers are breached.

High temperatures suppress defense sensors

Tomato plants and Arabidopsis thaliana Subjected to extreme heat, the expression of PRRs and RLKs, proteins involved in threat detection, decreases. Intense heat affects immunity, but the process of thermal acclimation can partially reverse this situation.

Acclimation, induced by gradual exposure to heat, stimulates the action of HSF family transcription factors. In particular, HSFA2 and HSFA3 activate sensor genes such as FLS2, EFR, and PEPR1. This mechanism allows plants to respond better to infections in hot environments.

Cold strengthens PRRs but suppresses damage sensors

Exposure to cold (4°C) alters the expression of immune genes. Studies with Arabidopsis show an increase in receptors such as FLS2, BAK1, and FRK1. On the other hand, cell integrity sensors, such as WAKs and PEPRs, are suppressed.

Cold activates transcription factors such as DREB1 and CAMTA3. These regulators interact with NPR1, a key salicylic hormone receptor, amplifying the immune response. The response is coordinated with resistance genes such as WRKY46 and PR2.

Water stress has ambiguous effects

Drought affects immunity in varying ways. In some situations, it induces resistance. In others, it increases susceptibility.

In Arabidopsis, moderate drought suppresses salicylic acid-regulated defense genes via activation of the water stress hormone ABA. However, during recovery from drought, the phenomenon of "rehydration-induced immunity" (DRII) occurs, with reactivation of receptors such as FLS2 and PEPR1.

Furthermore, sensors such as CRKs and THE1 increase their expression after exposure to dry air. This effect suggests that plants perceive cellular damage caused by lack of water and activate defense mechanisms.

Combined stress confuses the immune system

When heat and drought occur simultaneously, responses become unpredictable. Some reactions combine, others cancel each other out. In experiments with barley, the combination led to greater genetic reprogramming than either stress alone. Even so, immune gene expression was lower, indicating suppression of the defense system.

This blockage may be related to the dominance of ABA signaling, which negatively interferes with the salicylic acid and jasmonate pathways — essential for immunity.

Implications for agriculture

The findings reinforce that plants' surface sensors are directly influenced by environmental conditions. Cold activates PRRs and inhibits damage sensors. Extreme heat suppresses both. Drought causes contradictory effects, but rehydration reactivates the defense system.

Two groups of transcription factors stand out: HSFs, linked to heat, and DREBs, associated with cold. Both act at the intersection of abiotic stress and immunity, regulating genes such as FLS2 and EDS1.

Paths to the future

As climate change intensifies, identifying the molecular regulators that control immunity under stress becomes a priority. Technologies such as RNA-seq, ChIP-seq, and ATAC-seq should be applied to map the interaction between DNA and transcription factors under different environmental conditions.

Furthermore, tools like molecular modeling and machine learning can help predict how defense receptors behave in adverse scenarios. This data will enable the development of more resistant cultivars and protection strategies that work outside the laboratory.

Further information at doi.org/10.1016/j.tplants.2025.07.009