The Septin Gene Contributes to the Pathogenicity of by Regulating the Morphology, Cell Wall Integrity, and Pathogenic Factor Biosynthesis.

Septins are a conserved group of GTP-binding proteins found in all eukaryotes and are the fourth-most abundant cytoskeletal proteins. Septins of some pathogenic fungi are involved in morphological changes related to infection. Our previous studies have identified four core septins (-) in , the causal agent of northern corn leaf blight, while only is significantly upregulated during the invasive process. We therefore used forchlorfenuron (FCF), the specific inhibitor of septin, and Δ knockout mutants to further clarify the role of septins in pathogenicity. FCF treatment caused a dose-dependent reduction in colony growth, delayed the formation of infection structures, and reduced the penetration ability. Δ knockout mutants displayed abnormal mycelium morphology, slow mycelial growth, conidiation deficiency, delayed appressorium development, and weakened pathogenicity. deletion also broke cell wall integrity, altered chitin distribution, decreased the melanin content, and disrupted normal nuclear localization. A transcriptomic comparison revealed that genes differentially expressed between Δ and WT were enriched in terms of ribosomes, protein translation, membrane components, and transmembrane transport activities. Our results demonstrate that is required for morphology and pathogenicity in , making it a promising target for the development of novel fungicides.