Colletotrichum gloeosporioides is a hemibiotrophic ascomycete fungus that causes anthracnose on numerous plants worldwide and forms a specialized infection structure known as an appressorium in response to various plant surface signals. However, the associated mechanism of host surface signal recognition remains unclear. In the present study, three putative sensors, namely the mucin Msb2, the membrane sensor protein Sho1, and the G-protein-coupled receptor Pth11, were identified and characterized. The results showed that CgMsb2 plays a major role in the recognition of various host surface signals; deletion of CgMsb2 resulted in significant defects in appressorium formation, appressorium penetration, cellophane membrane penetration, and pathogenicity. CgSho1 plays a minor role and together with CgMsb2 cooperatively regulates host signal recognition, cellophane membrane penetration, and pathogenicity; deletion of CgSho1 resulted in an expansion defect of infection hyphae. Deletion of CgPth11 in wildtype, ΔCgMsb2, and ΔCgSho1 strains only resulted in a slight defect in appressorium formation at the early stage, and CgPth11 was dispensable for penetration and pathogenicity. However, exogenous cAMP failed to restore the defect of appressorium formation in ΔCgPth11 at the early stage. CgMsb2 contributed to the phosphorylation of the mitogen-activated protein kinase CgMk1, which is essential for infection-associated functions, while CgSho1 was unable to activate CgMk1 alone but rather cooperated with CgMsb2 to activate CgMk1. These data suggest that CgMsb2 contributes to the activation of CgMk1 and has overlapping functions with CgSho1 in plant surface sensing, appressorium formation, and pathogenicity.

中文翻译：

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粘蛋白Msb2与跨膜蛋白Sho1协同作用于杨树炭疽病菌Colletotrichum gloeosporioides的各种植物表面信号传感和致病过程

Colletotrichum gloeosporioides是一种半营养子囊菌类真菌，在世界范围内引起许多植物的炭疽病，并形成一种特殊的感染结构，称为附着体，以响应各种植物表面信号。然而，宿主表面信号识别的相关机制仍不清楚。在本研究中，鉴定和表征了三种假定的传感器，即粘蛋白 Msb2、膜传感器蛋白 Sho1 和 G 蛋白偶联受体 Pth11。结果表明，CgMsb2在多种宿主表面信号的识别中起主要作用；删除CgMsb2导致附着胞形成、附着胞穿透、玻璃纸膜穿透和致病性的显着缺陷。CgSho1 起次要作用，与 CgMsb2 共同调节宿主信号识别、玻璃纸膜穿透和致病性；CgSho1的缺失导致感染菌丝的扩张缺陷。野生型、ΔCgMsb2和ΔCgSho1菌株中CgPth11的缺失仅导致早期附着胞形成的轻微缺陷，而CgPth11对于渗透和致病性是可有可无的。然而，外源 cAMP 未能恢复 ΔCgPth11 中附着胞形成的缺陷在早期阶段。CgMsb2 有助于丝裂原活化蛋白激酶 CgMk1 的磷酸化，这对于感染相关功能至关重要，而 CgSho1 不能单独激活 CgMk1，而是与 CgMsb2 合作激活 CgMk1。这些数据表明，CgMsb2 有助于 CgMk1 的激活，并且在植物表面传感、附着胞形成和致病性方面与 CgSho1 具有重叠功能。