Sterol Regulatory Element-Binding Protein Sre1 Mediates the Development and Pathogenicity of the Grey Mould Fungus Botrytis cinerea

The grey mould fungus <i>Botrytis cinerea</i> is a dangerous plant pathogen responsible for substantial agricultural losses worldwide. The pathogenic mechanisms still have many unclear aspects, and numerous new pathogenic genes remain to be identified. Here, we show that the sterol regulatory element-binding protein Sre1 plays an important role in the development and pathogenicity of <i>B. cinerea</i>. We identified a homologue of gene <i>SRE1</i> in the <i>B. cinerea</i> genome and utilized a reverse genetics approach to create the knockout mutant Δ<i>sre1</i>. Our results demonstrate that <i>SRE1</i> is essential for conidiation, as Δ<i>sre1</i> produced only 3% of the conidia compared to the wild-type strain. Conversely, Δ<i>sre1</i> exhibited increased sclerotium production, indicating a negative regulatory role of <i>SRE1</i> in sclerotium formation. Furthermore, ergosterol biosynthesis was significantly reduced in the Δ<i>sre1</i> mutant, correlating with increased sensitivity to low-oxygen conditions. Pathogenicity assays revealed that Δ<i>sre1</i> had significantly reduced virulence, although it maintained normal infection cushion formation and penetration capabilities. Additionally, <i>SRE1</i> was found to be crucial for hypoxia adaptation, as Δ<i>sre1</i> showed abnormal germination and reduced growth under low-oxygen conditions. These findings suggest that <i>SRE1</i> mediates the development and pathogenicity of <i>B. cinerea</i> by regulating lipid homeostasis and facilitating adaptation to host tissue environments.