The role of the transcription factor FsBrlA in regulating sporulation, cell wall integrity stress response, and pathogenicity in Fusarium solani.

BrlA is a multifunctional transcription factor identified in specific clades of filamentous fungi, notably within the Hyphomycetes. It is widely involved in sporulation, cell wall stress response and pathogenicity, and plays an important role in fungal growth and development. To investigate the biological function of the FsbrlA in Fusarium solani, this study employed a split-marker homologous recombination strategy to directionally construct FsbrlA knockout and complementation strains. Through analyses of growth and development phenotypes, determination of cell wall components and trehalose content, abiotic stress treatments, and pathogenicity assays, the biological functions of the FsbrlA were systematically elucidated. The study findings indicate that FsbrlA deletion down-regulates the expression of key sporulation genes in F. solani, resulting in a 93.9% reduction in spore production and a 96.4% decrease in spore germination rate. It also leads to increased aerial mycelium length and reduced surface hydrophilicity. The deletion of FsbrlA also disrupts cell membrane structure, reduces the content of key cell wall components chitin, cellulose, and β-1, 3-glucan, and inhibits the biosynthesis of the stress response compound trehalose. This leads to increased susceptibility of the mutant strain to various stresses, particularly cell wall stress. In addition, ΔFsbrlA mutant also showed significantly reduced pathogenicity on wolfberry plants. In summary, loss of FsbrlA leads to impaired sporulation, altered stress sensitivity, and reduced pathogenicity, suggesting its involvement in these biological processes in F. solani. This study provides preliminary evidence for understanding the biological functions of the FsBrlA protein in F. solani and for exploring the potential mechanisms regulating its growth, development, and pathogenicity.