<p>Climate change is rapidly altering fruit crop pathosystems, accelerating coevolutionary dynamics between hosts and pathogens. This review synthesizes key mechanisms through which climatic factors, particularly temperature, influence virulence adaptation in fruit crops. For instance, <i>Colletotrichum gloeosporioides</i> shows a&#xa0;4.8-day reduction in latency per +1 °C increase in temperature for mangoes, while <i>Xanthomonas citri</i> hijacks its <i>XopAM-HSP40</i> chaperone to degrade <i>MnNLRX1</i> immunity in citrus fruits above 32 °C. In addition to temperature, other abiotic stressors such as drought (Ψs &lt; −2.5 MPa) impair physiological defenses in citrus by suppressing CsBPR1 expression through ROS-mediated histone hyperacetylation. Elevated CO<sub>2</sub> (780 ppm) disrupts SA-JA cross-talk, leading to a&#xa0;73% increase in strawberry susceptibility to <i>Botrytis cinerea</i>. Critically, these climatic factors induce phenological mismatches, escalating the risk of epidemics. For example, <i>Venturia inaequalis</i> ascospore discharge peaks 9.3&#xa0;days earlier per 1 °C of warming, misaligning conventional fungicide application timings. Emerging solutions leverage cutting-edge multi-omics technologies. CRISPR-<i>MdJMJ14</i> epigenome editing stabilizes apple NLR clusters under heat stress (&gt; 35 °C), reducing scab penetration by 64%. Chitosan-γ-PGA nanoemulsions enable circadian-triggered salicylic acid (SA) release during <i>Erysiphe necator</i> conidiation peaks. Furthermore, PhytoRisk 4.0&#xa0;digital twins integrate stochastic climate modeling with ascospore maturation phytobiometers (AUC = 0.91), reducing fungicide use by 32%. These innovations contribute to the development of integrated resilience ecosystems, where biochar–Streptomyces consortia sequester 3.8 t&#xa0;C/ha and year and suppress <i>Phytophthora</i> via <i>β‑1, 3</i>‑glucanase induction (+4.2 U/mg). Future research priorities include deciphering vector–pathogen metabolome crosstalk (e.g., <i>Diaphorina citri</i> gut metatranscriptomics), developing phytoanticipin chronotherapy for circadian defense priming, and advancing policy frameworks that monetize carbon-negative disease suppression. Urgent interdisciplinary collaboration is essential to ensure the resilience of global fruit production against climate-induced disease threats.</p> Graphic abstract <p></p>

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Climate Change Impacts on Fruit Crops and Mechanisms of Stress-Induced Disease Dynamics for Resilience Strategies

  • Muhammad Umer Iqbal,
  • Syed Atif Hasan Naqvi

摘要

Climate change is rapidly altering fruit crop pathosystems, accelerating coevolutionary dynamics between hosts and pathogens. This review synthesizes key mechanisms through which climatic factors, particularly temperature, influence virulence adaptation in fruit crops. For instance, Colletotrichum gloeosporioides shows a 4.8-day reduction in latency per +1 °C increase in temperature for mangoes, while Xanthomonas citri hijacks its XopAM-HSP40 chaperone to degrade MnNLRX1 immunity in citrus fruits above 32 °C. In addition to temperature, other abiotic stressors such as drought (Ψs < −2.5 MPa) impair physiological defenses in citrus by suppressing CsBPR1 expression through ROS-mediated histone hyperacetylation. Elevated CO2 (780 ppm) disrupts SA-JA cross-talk, leading to a 73% increase in strawberry susceptibility to Botrytis cinerea. Critically, these climatic factors induce phenological mismatches, escalating the risk of epidemics. For example, Venturia inaequalis ascospore discharge peaks 9.3 days earlier per 1 °C of warming, misaligning conventional fungicide application timings. Emerging solutions leverage cutting-edge multi-omics technologies. CRISPR-MdJMJ14 epigenome editing stabilizes apple NLR clusters under heat stress (> 35 °C), reducing scab penetration by 64%. Chitosan-γ-PGA nanoemulsions enable circadian-triggered salicylic acid (SA) release during Erysiphe necator conidiation peaks. Furthermore, PhytoRisk 4.0 digital twins integrate stochastic climate modeling with ascospore maturation phytobiometers (AUC = 0.91), reducing fungicide use by 32%. These innovations contribute to the development of integrated resilience ecosystems, where biochar–Streptomyces consortia sequester 3.8 t C/ha and year and suppress Phytophthora via β‑1, 3‑glucanase induction (+4.2 U/mg). Future research priorities include deciphering vector–pathogen metabolome crosstalk (e.g., Diaphorina citri gut metatranscriptomics), developing phytoanticipin chronotherapy for circadian defense priming, and advancing policy frameworks that monetize carbon-negative disease suppression. Urgent interdisciplinary collaboration is essential to ensure the resilience of global fruit production against climate-induced disease threats.

Graphic abstract