Integrated transcriptomic and metabolomic dynamics reveal mechanisms of tobacco resistance to Phytophthora nicotianae.

Metabolome profiling reveals the resistance mechanisms of rice against brown planthopper.

It is demonstrated that Bph6 mediates a more stable and effective defense metabolism in rice through coordinated regulation of primary and secondary metabolism, particularly flavonoid- and serotonin-related pathways.

Combined transcriptomics and metabolomics reveals the molecular mechanism by which rice responds to Ustilaginoidea virens infection.

The combined transcriptome and metabolome analysis revealed that plant hormone signal transduction, phenylpropanoid biosynthesis, and flavonoid biosynthesis were significantly enriched in resistant rice varieties, providing valuable information on the molecular mechanisms by which rice defends against U. virens infection.

Integrated Analysis of Transcriptomic and Metabolomic Responses in Rice Resisting False Smut

Integrated transcriptome and metabolome analysis of resistant and susceptible tomato cultivars in response to tomato mottle mosaic virus and functional characterization of snakin-2 in viral defense.

Assays demonstrated that SlSN2 overexpression suppressed ToMMV accumulation and infection, likely via enhanced lignin biosynthesis, suggesting a potential role for SlSN2 in contributing to ToMMV resistance, independent of the known Tm‑2² pathway.

Spatiotemporal metabolomics of tobacco leaves in response to Pseudomonas syringae infection

Abstract Tobacco (Nicotiana tabacum L.) is a major economic crop and a model for plant–pathogen interactions, yet the spatiotemporal dynamics of defense metabolism during infection remain poorly characterized. Here, we used MALDI-MSI-based spatial metabolomics to systematically profile tobacco leaves during Pseudomonas syringae infection. Multidimensional analysis of 1,399 annotated metabolites revealed distinct spatiotemporal regulation patterns. Temporally, early infection (12 h postinfection (hpi)) was characterized by increased organic acids and terpenoids, followed by a mid-stage shift toward phenolic acids and quinones (24 hpi) and a late-stage enrichment of alkaloids by 60 hpi. Spatially, constrained clustering produced anatomy-aligned segmentation maps and revealed cell type preferences across epidermal, mesophyll, and vascular regions, with directional redistribution of differentially expressed metabolites as infection progressed. Defense hormones, including salicylic acid (SA) and jasmonic acid (JA), preferentially accumulated in vascular bundles and varied dynamically over time. Functional validation through exogenous application of representative metabolites (eg calystegine C1 and L-phenylalanine) and hormones (JA and SA), together with genetic manipulation of JA-biosynthetic genes, confirmed their roles in reducing lesion development and suppressing bacterial proliferation. Notably, epidermal enrichment of alkaloids—especially nicotine—and amino acid derivatives showed a decrease-then-increase pattern consistent with early consumption and later replenishment; nicotine's defensive contribution was further supported using a low-nicotine mutant. Collectively, P. syringae infection orchestrates a coordinated, cell type-compartmentalized defense metabolic program in tobacco, providing a resource for mechanistic studies and metabolic engineering of disease resistance. This time- and tissue-resolved atlas links metabolite remodeling to hormone-associated signaling and chemical barrier formation during wildfire disease progression.

Disease-stage-associated transcriptional responses underlying bacterial wilt resistance in tobacco cultivar Yunyan 87 caused by Ralstonia solanacearum.

Bacterial wilt caused by Ralstonia solanacearum severely limits tobacco production, yet the molecular basis of resistance to vascular wilt diseases remains poorly understood. We integrated field phenotyping, pathogen isolation, and transcriptomic analyses across different disease stages to investigate root responses of the resistant tobacco cultivar Yunyan 87 at healthy, moderately infected, and severely infected stages. Disease progression was accompanied by marked root biomass loss, with fresh and dry weights reduced by approximately 60% and 70%, respectively. Transcriptomic analyses identified 994 up-regulated and 1,151 down-regulated genes at the moderate stage, and 2,158 up-regulated and 2,284 down-regulated genes at the severe stage. WGCNA identified a disease severity-associated regulatory module. Functional enrichment analyses showed that moderate infection activated stress perception and redox homeostasis, whereas severe infection strongly suppressed translation and ribosome biogenesis. Dynamic expression pattern analysis further revealed coordinated activation of phenylpropanoid metabolism and lignin biosynthesis, and synergistic induction of MAPK, salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) signaling pathways, followed by progressive metabolic repression. Key transcription factor families, including WRKY, MYC2, and ERF, exhibited distinct stage-dependent expression patterns. Collectively, our results demonstrate a disease-stage-associated transcriptional reprogramming strategy that balances defense activation and metabolic restraint during bacterial wilt progression, providing valuable regulatory networks and candidate genes for breeding tobacco cultivars with enhanced resistance.