The tomato is a fruit vegetable rich in nutritional and medicinal value grown in greenhouses and fields worldwide. It is severely sensitive to heat stress, which frequently occurs with rising global warming. Predictions indicate a 0.2 °C increase in average surface temperatures per decade for the next three decades, which underlines the threat of austere heat stress in the future. Previous studies have reported that heat stress adversely affects tomato growth, limits nutrient availability, hammers photosynthesis, disrupts reproduction, denatures proteins, upsets signaling pathways, and damages cell membranes. The overproduction of reactive oxygen species in response to heat stress is toxic to tomato plants. The negative consequences of heat stress on the tomato have been the focus of much investigation, resulting in the emergence of several therapeutic interventions. However, a considerable distance remains to be covered to develop tomato varieties that are tolerant to current heat stress and durable in the perspective of increasing global warming. This current review provides a critical analysis of the heat stress consequences on the tomato in the context of global warming, its innate response to heat stress, and the elucidation of domains characterized by a scarcity of knowledge, along with potential avenues for enhancing sustainable tolerance against heat stress through the involvement of diverse advanced technologies. The particular mechanism underlying thermotolerance remains indeterminate and requires further elucidatory investigation. The precise roles and interplay of signaling pathways in response to heat stress remain unresolved. The etiology of tomato plants’ physiological and molecular responses against heat stress remains unexplained. Utilizing modern functional genomics techniques, including transcriptomics, proteomics, and metabolomics, can assist in identifying potential candidate proteins, metabolites, genes, gene networks, and signaling pathways contributing to tomato stress tolerance. Improving tomato tolerance against heat stress urges a comprehensive and combined strategy including modern techniques, the latest apparatuses, speedy breeding, physiology, and molecular markers to regulate their physiological, molecular, and biochemical reactions.

Bacterial wilt (BW) is a globally serious soil-borne disease in a wide range of plants, caused by diverse strains of Ralstonia solanacearum. However, there are few research reports on melatonin regulating plant resistance against R. solanacearum. N-acetyltransferase SlSNAT2 is a rate-limiting enzyme in plant melatonin synthesis. This study elucidates the mechanisms of SlSNAT2 modulating tomato resistance to BW. SlSNAT2 was expressed in tomato roots, stems, and leaves and induced upon R. solanacearum inoculation. Knocking out SlSNAT2 significantly decreased the melatonin content in CRISPR/Cas9 mutant slsnat2. With R. solanacearum inoculation, the morbidity and disease index value of slsnat2 were significantly higher than those of the tomato wild-type plant Micro-Tom (MT) according to the wilt rate and severity. The chlorophyll levels, photosynthetic rates, and callus deposition quantity in slsnat2 were notably lower while the reactive oxygen species (ROS) level was considerably higher than those in the MT after inoculation. Additionally, the SlSNAT2 deficiency depressed the expression of the mitogen-activated protein kinase (MAPK) pathway genes (SlMPK1, SlMKK2), salicylic acid pathway genes (SlGluA, SlPR-1a), jasmonic acid pathway gene SlPin2, and pathogenesis-related (PR) protein genes (SlPR-STH2a, SlPR-STH2b, SlPR-STH2c, SlPR-STH2d). These results revealed SlSNAT2 enhanced the tomato resistance against R. solanacearum by orchestrating ROS homeostasis, callose deposition, MAPK signaling, hormone pathways, and PR gene transcripts.