Sur7 is one of multiple proteins constituting MCC (membrane compartment of Can1 acting as an arginine/H⁺ symporter), a crucial membrane domain that can form punctuate eisosome spots on the plasma membrane and execute diverse functions in model yeast but remains poorly understood in filamentous fungi. Here, a Sur7 homolog bearing a typical SUR7 domain and four transmembrane domains was shown to localize in the conidial vesicles and enter vacuoles and appear sporadically on the periphery membrane during hyphal growth in the insect-pathogenic fungus Beauveria bassiana, implicating an involvement of Sur7 in cellular events linked to both plasma membrane and vacuoles. Deletion of sur7 resulted in reduced conidiation capacity and impaired conidial quality, which was featured by slower germination, attenuated virulence, and reduced carbohydrate epitopes (β-N-acetylglucosamine and sialic acids). Also, the hyphal cell walls of the deletion mutant were severely impaired due to ~ 70% reductions in chitin and neutral carbohydrate contents and a moderate increase in alkali-soluble carbohydrate content. Consequently, the deletion mutant became more sensitive to three cell wall perturbing chemicals (Congo red, calcofluor white, and SDS) and an antifungal drug (caspofungin) and surprisingly showed a hypersensitivity to oxidative stress of H₂O₂ and an increased sensitivity to osmotic stress of NaCl or sorbitol. Its hypersensitivity to H₂O₂ was associated with transcriptional repression of critical catalase genes required for H₂O₂ decomposition. These findings unveil that Sur7 takes part in both MCC/eisosome and vacuolar events and hence acts as a sustainer of conidiation capacity, cell wall integrity, multiple stress tolerance, and virulence in B. bassiana.

Sur7是构成MCC（Can1的膜区室，充当精氨酸/ H ⁺同向转运蛋白）的多种蛋白质之一，这是一种至关重要的膜结构域，可以在质膜上形成点状的同质体斑点，并在模型酵母中执行多种功能，但在丝状中仍然知之甚少菌类。在这里，显示出具有典型SUR7结构域和四个跨膜结构域的Sur7同源物位于分生孢子囊泡中并进入液泡，并在病原性真菌球孢白僵菌的菌丝生长过程中偶发地出现在外围膜上，这暗示了Sur7参与了细胞事件与质膜和液泡相关。删除sur7导致分娩能力降低和分生孢子质量受损，其特征是发芽速度变慢，毒力减弱和碳水化合物表位（β- N-乙酰氨基葡萄糖和唾液酸）降低。同样，由于几丁质和中性碳水化合物含量减少约70％，碱溶性碳水化合物含量适度增加，导致缺失突变体的菌丝细胞壁严重受损。因此，该缺失突变体对三种细胞壁干扰化学物质（刚果红，钙氟荧光白和SDS）和一种抗真菌药（卡泊芬净）变得更加敏感，并且令人惊讶地显示出对H ₂ O _2的氧化应激超敏性和对渗透压的敏感性增加。 NaCl或山梨糖醇的压力。对H ₂过敏O ₂与H ₂ O ₂分解所需的关键过氧化氢酶基因的转录抑制有关。这些发现表明，Sur7参与了MCC /同质体事件和液泡事件，因此在球孢白僵菌中具有分生能力，细胞壁完整性，多重胁迫耐受性和毒性。