Abstract
In phytopathogenic fungi, adhesion to plant substrates is followed by environmental sensing and the initiation of degradation processes. The mechanisms underlying substrate surface recognition are considered critical components of the pathogen's survival strategy. For instance, certain species of phytopathogenic fungi, such as Bipolaris maydis, develop specialized infection structures known as appressoria during infection that penetrate the host. Appressorium formation is triggered by the recognition of surface hydrophobicity and host-derived compounds. The ∆opy2 strain of B. maydis remains pathogenic but is deficient in recognizing hydrophobic surfaces and does not efficiently form appressoria on such surfaces. The addition of host-derived pectin induces appressorium formation in ∆opy2, but the underlying mechanism remains unclear. In this study, we isolated a mutant strain, D296, derived by mutating the ∆opy2 strain, which fails to form appressoria in response to pectin and had straight hyphae with fewer branches than the ∆opy2 strain following spore germination. Genetic crosses involving the wild-type strain, D296, and their progeny suggested that these phenotypes are controlled by a single gene. Whole-genome comparisons among wild-type and mutant progenies revealed a single-nucleotide polymorphism in a gene encoding an α/β-hydrolase that was associated with the observed traits. Introduction of the wild-type gene into the D296 strain restored both appressorium formation and hyphal morphology; we named this gene LAG1. In lag1-disrupted strains, elongated hyphae were similar to those in the D296 strain, appressorium formation on hydrophobic surfaces was significantly reduced, and pectin-induced appressorium formation was abolished. These results demonstrate that LAG1 plays a key role in appressorium formation in this fungus.
