Contribution of MylA in Conidiogenesis, Conidia Germination, and beta-Glucan Biosynthesis in Aspergillus fumigatus

Abstract

The conidia of Aspergillus fumigatus are the primary infectious propagules responsible for initiating invasive aspergillosis, and their development and physiology are closely regulated by numerous transcription factors. Our previous study demonstrated that the MYB-like transcription factor MylA plays a critical role in asexual sporulation and conidial viability in Aspergillus nidulans. However, the function of MylA in A. fumigatus has not yet been investigated. This study aimed to investigate the role of MylA, a member of the MYB-like transcription factor family, in conidiogenesis, conidial viability, cell wall integrity, and germination in A. fumigatus. Deletion of mylA resulted in reduced vegetative growth, abnormal conidiophore development, and a significant decrease in conidial production. Furthermore, ΔmylA conidia exhibited reduced trehalose accumulation, decreased viability, and increased sensitivity to heat and oxidative stress. Deletion of mylA also delayed conidial germination and impaired biofilm formation. Transcriptomic analysis of conidia identified approximately 2,200 differentially expressed genes, including those involved in β-glucan biosynthesis. Notably, deletion of mylA significantly upregulated the expression of fks1 and gel1, resulting in increased β-glucan accumulation in the conidial cell wall. Collectively, these findings demonstrate that MylA is a key regulator of conidiogenesis, conidial viability, germination, and β-glucan biosynthesis in A. fumigatus.