Wang Yixi, Xia Gengshou, Xie Xinyi, Wang Hao, Zheng Lingyun, He Zhijie, Ye Junxian, Xu Kangtong, Shi Qi, Yang Hui, Zhang Yan
Department of Landscape and Horticulture, Ecology College, Lishui University, Lishui 323000, China.
Int J Mol Sci. 2025 Jul 7;26(13):6530. doi: 10.3390/ijms26136530.
Bacterial wilt (BW) is a globally serious soil-borne disease in a wide range of plants, caused by diverse strains of . However, there are few research reports on melatonin regulating plant resistance against . -acetyltransferase SlSNAT2 is a rate-limiting enzyme in plant melatonin synthesis. This study elucidates the mechanisms of SlSNAT2 modulating tomato resistance to BW. was expressed in tomato roots, stems, and leaves and induced upon inoculation. Knocking out significantly decreased the melatonin content in CRISPR/Cas9 mutant . With inoculation, the morbidity and disease index value of 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 were notably lower while the reactive oxygen species (ROS) level was considerably higher than those in the MT after inoculation. Additionally, the deficiency depressed the expression of the mitogen-activated protein kinase (MAPK) pathway genes (, ), salicylic acid pathway genes (, ), jasmonic acid pathway gene , and pathogenesis-related (PR) protein genes (, , , ). These results revealed SlSNAT2 enhanced the tomato resistance against by orchestrating ROS homeostasis, callose deposition, MAPK signaling, hormone pathways, and PR gene transcripts.
青枯病(BW)是一种在全球范围内对多种植物造成严重危害的土传病害,由多种菌株引起。然而,关于褪黑素调节植物对青枯病抗性的研究报道较少。N-乙酰转移酶SlSNAT2是植物褪黑素合成中的限速酶。本研究阐明了SlSNAT2调节番茄对青枯病抗性的机制。SlSNAT2在番茄根、茎和叶中表达,并在青枯病菌接种后被诱导。敲除SlSNAT2显著降低了CRISPR/Cas9突变体中的褪黑素含量。接种青枯病菌后,根据萎蔫率和严重程度,SlSNAT2敲除突变体的发病率和病情指数值显著高于番茄野生型植株Micro-Tom(MT)。接种后,SlSNAT2敲除突变体的叶绿素水平、光合速率和胼胝质沉积量显著低于MT,而活性氧(ROS)水平则显著高于MT。此外,SlSNAT2缺失抑制了丝裂原活化蛋白激酶(MAPK)途径基因(MPK3、MPK6)、水杨酸途径基因(PR1、PR2)、茉莉酸途径基因PDF1.2和病程相关(PR)蛋白基因(PR1、PR2、PR5、PR10)的表达。这些结果表明,SlSNAT2通过协调ROS稳态、胼胝质沉积、MAPK信号传导、激素途径和PR基因转录本增强了番茄对青枯病的抗性。