Pathotype-specific roles of putative conidiation regulators in development, secondary metabolism, and pathogenicity...

Fusarium fujikuroi, the causal agent of rice bakanae disease, comprises two pathotypes with distinct symptoms: the fumonisin-producing blight type (B14) and the gibberellin-producing elongation type (B20). Asexual spore production and secondary metabolism are essential for disease transmission and development in F. fujikuroi, and conidiation regulators frequently influence secondary metabolism and other phenotypes in filamentous fungi. To investigate the genetic basis underlying differences between the two pathotypes, we generated deletion mutants for 14 genes corresponding to well-characterized conidiation regulators (upstream activators, central regulators, and velvet complex components) in both B14 and B20. Phenotypic analyses revealed that several upstream regulators, including FfflbD, are essential for macroconidiation in both strains, whereas others, such as FfflbA, FfflbB, and FfflbE, showed pathotype-dependent roles. The central regulator FfabaA was indispensable for conidiation in both backgrounds, while FfwetA displayed divergent roles in conidial maturation. Velvet regulators (Ffvel1, Ffvel2, and Fflae1) promoted conidiation in both backgrounds, with Fflae1 additionally affecting macroconidiation in B20. In B14, deletion of Ffvel1, Ffvel2, FfabaA, or FfwetA abolished or significantly reduced virulence and was associated with decreased FUM1 expression, linking conidiation with fumonisin biosynthesis and pathogenicity. In B20, several mutants partially shifted toward blight-like symptoms and altered gibberellin gene expression. Notably, ΔFflae1 in B20 caused >500-fold FUM1 upregulation, increased fumonisin accumulation to near-B14 levels, and induced blight-like disease symptoms. Transcriptional profiling across mutants revealed distinct regulatory network architectures between B14 and B20. Together, these results show extensive divergence in developmental regulatory networks between F. fujikuroi pathotypes and implicate chromatin-associated control in pathotype differentiation.