Molecular insights into Solanum sisymbriifolium’s resistance against Globodera pallida via RNA-seq

Abstract

Background The presence of potato cyst nematodes (PCN) causes a significant risk to potato crops globally, leading to reduced yields and economic losses. While the plant Solanum sisymbriifolium is known for its resistance to PCN and can be used as a trap crop, the molecular mechanisms behind this resistance remain poorly understood. In this study, genes differentially expressed were identified in control and infected plants during the early stages of the S. sisymbriifolium - G. pallida interaction. Results Gene expression profiles were characterized for two S. sisymbriifolium cultivars, Melody and Sis6001, uninfected and infected by G. pallida . The comparative transcriptome analysis revealed a total of 4,087 and 2,043 differentially expressed genes (DEGs) in response to nematode infection in the cultivars Melody and Sis6001, respectively. Gene ontology (GO) enrichment analysis provided insights into the response of the plant to nematode infection, indicating an activation of the plant metabolism, oxidative stress leading to defence mechanism activation, and modification of the plant cell wall. Genes associated with the jasmonic and salicylic acid pathways were also found to be differentially expressed, suggesting their involvement in the plant’s defence response. In addition, the analysis of NBS-LRR domain-containing transcripts that play an important role in hypersensitive response and programmed cell death led to the identification of ten transcripts that had no annotations from the databases, with emphasis on TRINITY_DN52667_C1_G1, found to be upregulated in both cultivars. Conclusions These findings represent an important step towards understanding the molecular basis underlying plant resistance to nematodes and facilitating the development of more effective control strategies against PCN. Supplementary Information The online version contains supplementary material available at 10.1186/s12870-024-05694-1.