Int J Mol Sci. 2025 Jul 7;26(13):6530. doi: 10.3390/ijms26136530.
ABSTRACT
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.
PMID:40650305 | DOI:10.3390/ijms26136530
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