Genome Editing for Biotic and Abiotic Stress Resistance in Tomato: Advances Enabled by CRISPR/Cas Systems

Abstract

Tomato (Solanum lycopersicum) faces increasing pressure from both biotic threats, including bacterial, fungal, and viral pathogens, and abiotic stresses such as drought, salinity, heat, and cold, all of which substantially reduce productivity under changing climatic conditions. CRISPR/Cas-based genome editing has emerged as a powerful platform for elucidating stress-response mechanisms and accelerating the development of resilient tomato cultivars. This review summarizes recent advances in CRISPR-mediated engineering of both disease resistance and abiotic stress tolerance in tomato. For biotic resistance, we discuss susceptibility gene disruption, negative regulator knockout, and host-factor targeting strategies against major bacterial, fungal, and viral pathogens, including Pseudomonas syringae, Ralstonia solanacearum, Xanthomonas spp., TYLCV, and ToBRFV. For abiotic stress tolerance, we examine editing of regulatory networks controlling ion homeostasis, osmotic adjustment, ROS detoxification, hormonal signalling, and transcriptional regulation. We further evaluate delivery strategies, including Agrobacterium-mediated transformation, viral vectors, nanoparticle-assisted systems, and ribonucleoprotein (RNP) delivery, together with their implications for editing efficiency and transgene-free breeding. Emerging technologies such as base editing, prime editing, and multiplex CRISPR systems are highlighted for their capacity to fine-tune stress-associated alleles and regulatory pathways. Collectively, CRISPR-based technologies are advancing an integrated and mechanism-driven framework, linking perturbation data with transcriptomic, metabolomic, and epigenomic datasets, for improving both biotic resistance and abiotic stress resilience in tomato breeding programs. Oxidative stress is treated here not as an independent stress category but as a shared downstream ROS-mediated signal connecting these stress responses.