Modulation of key sterol-related genes of Nicotiana benthamiana by phosphite treatment during infection with Phytophthora cinnamomi

Phytophthora cinnamomi is a globally destructive pathogen causing disease in over 5000 plant species. As sterol auxotrophs, Phytophthora species rely on host-derived phytosterols for reproduction, yet the effects of pathogen infection on plant sterol biosynthesis remains unclear. We utilised a soil-free plant growth system to analyze the impacts of P. cinnamomi on Nicotiana benthamiana roots, a new model for studying P. cinnamomi–plant root interactions. Our results show that P. cinnamomi successfully infected all ecotypes tested, but infection was inhibited by the systemic chemical, phosphite. While phosphite is traditionally associated with the activation of plant defence mechanisms, we show that phosphite also modulates plant immune receptors and phytosterol biosynthesis. qPCR analyses revealed a two-fold upregulation of the N. benthamiana elicitin receptor, Responsive to Elicitins (REL), and its co-receptor, suppressor of BIR1-1 (SOBIR) during P. cinnamomi infection when compared with infected, phosphite-treated plants. Furthermore, key genes related to plant sterol biosynthesis were upregulated in their expression during pathogen infection but were suppressed in phosphite-treated and infected plants. Notably, the cytochrome P450 family 710 (CYP710A) gene encoding a C22-sterol desaturase, involved in stigmasterol production, a phytosterol known to be linked to plant susceptibility to pathogens, was downregulated in phosphite-treated plants, independent of infection status. These findings reveal novel insights into the role of phosphite in modulating plant immune responses and sterol metabolism, with potential in managing diseases caused by P. cinnamomi.