Characterization of the G protein-coupled receptor FfGpr1-Gα-AC signal transduction in Fusarium fujikuroi and its role in gibberellin biosynthesis

Abstract Aims This study aimed to characterize the G protein-coupled receptor FfGpr1-Gα-AC transduction pathway and its role in regulating gibberellin (GA) metabolism in Fusarium fujikuroi. Methods and results By constructing Ffgpr1 deletion and constitutively activated FfG2Q204 L mutants, we found that glucose-induced cAMP (cyclic Adenosine MonoPhosphate) synthesis was abolished in Ffgpr1Δ. Bimolecular fluorescence complementation confirmed membrane-localized FfGpr1-FfG2 and FfG2-AC interactions, with intensified fluorescence at septa. Fermentation assays revealed opposing GA3 yields: Ffgpr1Δ produced 21% less GA3 than the wild type, whereas FfG2Q204 L increased yield by 17%. qPCR（quantitative real-time PCR） analysis demonstrated that Ffgpr1Δ upregulated FfCPS/KS, FfP450-2, and FfP450-3 transcription by 6–8-fold while downregulating FfDES by 82%, whereas FfG2Q204 L induced a 6-fold increase in FfCPS/KS mRNA level. Strikingly, FfDES overexpression in Ffgpr1Δ restored GA3 production to wild-type levels but led to GA7 accumulation and suppressed FfP450-3 upregulation, suggesting feedback-regulated metabolic constraints. Conclusion Glucose-induced cAMP production required FfGpr1. FfGpr1-FfG2 and FfG2-AC interacted on the cell membrane, with enhanced co-localization at the septal region. The FfGpr1-Gα-AC pathway significantly affected GA yield, with complex and noteworthy regulation of GA cluster gene expression.