G-protein-coupled receptor sensing of farnesol controls fungal dormancy and is susceptible to bacterial interference.

Conidial dormancy is a critical survival strategy for fungi under stress, yet the mechanisms governing the switch between dormancy and germination remain unclear. Here we identify the G-protein-coupled receptor, Rsd1, as a farnesol-responsive sensor controlling this dormancy switch in the plant pathogen Fusarium pseudograminearum, which causes Fusarium crown rot. Under high population density and nutrient limitation, endogenous farnesol activates Rsd1 and downstream signalling pathways to suppress conidial germination. Rsd1 also responds to extracellular farnesol, linking environmental signals to an intrinsic transcriptional programme for dormancy. This adaptive response enhances survival but creates a fitness trade-off during plant infection. Specific rhizosphere-associated bacteria also contribute by promoting or inhibiting germination of dormant conidia through farnesol-Rsd1 sensing. Consortia assembled from these bacteria altered the balance between stress-resilient dormancy and infection-associated germination, thereby modulating disease severity. Our findings demonstrate how microbial interactions reshape intrinsic fungal regulatory programmes governing dormancy and infection.