Cucumber (Cucumis sativus L.) Fusarium wilt (FW), caused by Fusarium oxysporum f. sp. cucumerinum (Foc), is a devastating disease that significantly impacts cucumber production worldwide. The lack of natural resistant cultivars to FW has hindered the development of resistant cucumber varieties through conventional breeding methods. Interestingly, the disruption of susceptibility (S) genes has emerged as an effective alternative approach for enhancing crop resistance. Here, we identified a proline-rich nuclear receptor coactivator CsPNRC1 through transcriptomic analysis, and function as a susceptibility gene of cucumber FW using virus-induced gene silencing (VIGS), CRISPR/Cas- and overexpression-based methods. Seedlings overexpressing CsPNRC1 exhibited browning at the shoot bases 7 days after inoculation with Foc pathogens, while knockout seedlings demonstrated significantly greater resistance compared with wild-type (WT) plants. We identified CsPNRC1 interacting with a fasciclin-like arabinogalactan protein Csfla15 through yeast two-hybrid (Y2H) assays, bimolecular fluorescence complementation (BiFC), Co-immunoprecipitation (Co-IP), and luciferase complementation imaging (LCI) assay, and found that Csfla15 was regulated by CsPNRC1. Also, CsPNRC1 could influence the content of cell wall components pectin and cellulose in cucumber roots. Meanwhile, these findings provide valuable insights into the role of CsPNRC1 in cucumber's susceptibility to FW and highlight its potential use for resistance breeding.
Dong et al. (Wed,) studied this question.