This study conducted a transcriptomic analysis of in response to C. deformans infection in Picea schrenkiana, laying the foundation for future research into the molecular pathogenic mechanisms of C. deformans pathogenicity.

Using RNA-Seq technology to compare diseased and healthy current-year tissues of P. schrenkiana, this study explored the key genes, signaling pathways, and metabolic pathways involved in the P. schrenkiana - C. deformans interaction.

1) Transcriptome sequencing identifies 3 461 differentially expressed genes (DEGs), including 1 658 upregulated and 1 803 downregulated genes; 2) GO analysis shows that DEGs are mainly enriched in terms like transferase activity, sugar group transfer, heme binding, tetrapyrrole binding, ADP binding, coenzyme binding, iron ion binding, UDP-glycosyltransferase activity, and oxidoreductase activity; 3) KEGG analysis finds DEGs annotated in 124 KEGG pathways, with the most in metabolic pathways. DEGs are notably enriched in phenylpropanoid biosynthesis, flavonoid biosynthesis, glutathione metabolism, linoleic acid metabolism, and inositol phosphate metabolism pathways; 4) Terpene synthase-related genes LOC131073238, TPS-1, 8cin, TPS-Lin-2, PT5 (novel.5099) and PT5 (novel.5096) are downregulated, while LOC131042632 and ag5 are upregulated. Notably, DEGs LOC131042632, LOC131073238, and TPS-1,8cin are enriched in diterpenoid biosynthesis pathways; 5) In the phenylpropanoid biosynthesis pathway, DEGs CYP71AU50, PER12, PER53, PER65, 4CL, UGT84A2, and CCL7 are downregulated, while 36 DEGs are upregulated.

P. schrenkiana may respond to rust infection through strategies such as lignin synthesis, terpenoid compound production, and modulation of signaling transduction capabilities.

Utilizing non-targeted metabolomics technology to investigate the impact of Chrysomyxa deformans (Diet.) Jacz. on the metabolites of P.schrenkiana. The findings aim to provide a theoretical basis for the prevention and control of rust disease in P.schrenkiana.

In this study, current-year healthy and diseased P. schrenkiana shoots and leaves were collected, a non-targeted metabolomics study was conducted using liquid chromatography-mass spectrometry (LC-MS) technology. The differences in metabolites between healthy and diseased P. schrenkiana were compared, thresholds of P > 1.0, fold change > 1.500 or fold change < 0.667 and P < 0.05 were set for screen differential metabolites and the metabolic pathways were annotated through the KEGG database. Furthermore, in-depth analysis of the folate biosynthesis pathway, the diterpenoid biosynthesis pathway, and the butyrate metabolism pathway was conducted.

Significant differences were observed in the metabolites of healthy and diseased P.schrenkiana. There were 570 and 418 significantly different metabolites (SDMs) in the positive and negative ion modes, respectively. The differential metabolic products were mainly annotated to environmental information processing, genetic information processing, and metabolic pathways. Data analysis from the KEGG bubble chart indicated that the folate biosynthesis pathway, diterpenoid biosynthesis pathway, and butyrate metabolism pathway played crucial roles in the pathogenesis process of the pathogen on the host.

Rust fungus infection significantly affects the metabolites of P. schrenkiana, and metabolomics analysis suggests that the pathogen may trigger the occurrence of P. schrenkiana rust disease through changes in major secondary metabolites in the folate metabolism pathway, butyrate metabolism pathway, and diterpene biosynthesis pathway.