Curtis Erin R, Lew Daniel J
Biology Department, Massachusetts Institute of Technology, Cambridge, MA 02139.
bioRxiv. 2025 Aug 13:2025.08.12.669915. doi: 10.1101/2025.08.12.669915.
The fungal cell wall is constantly remodeled to allow cell growth, but any holes in the cell wall would lead to catastrophic lysis. The "Cell Wall Integrity" pathway (CWI) detects cell wall defects and promotes cell wall thickening or repair to protect cell integrity. However, cell walls must be removed at contact sites between fusing cells during mating or mycelium formation. Here we show that in , the CWI is downregulated specifically at the contact site between mating cells. A key component of the CWI, Pkc1, accumulated at polarity sites (shmoo tips) in cells exposed to mating pheromone, but not at contact sites. Pkc1 exclusion required a cell wall protein, Fig2, induced by pheromone. In mutants lacking Fig2, cell wall removal was delayed, blocked, or even reversed after transient fusion, leading to reduced mating. These results suggest that Fig2 designates the contact site as a "safe" spot to degrade the cell wall.
真菌细胞壁会不断重塑以允许细胞生长，但细胞壁上的任何孔洞都会导致灾难性的细胞裂解。“细胞壁完整性”途径（CWI）可检测细胞壁缺陷，并促进细胞壁增厚或修复以保护细胞完整性。然而，在交配或菌丝体形成过程中，融合细胞之间的接触部位的细胞壁必须被去除。在这里我们表明，在[具体物种或菌株未提及]中，CWI在交配细胞之间的接触部位特异性下调。CWI的一个关键成分Pkc1，在暴露于交配信息素的细胞中的极性位点（芽体尖端）积累，但不在接触部位积累。Pkc1的排除需要一种由信息素诱导的细胞壁蛋白Fig2。在缺乏Fig2的突变体中，细胞壁去除在短暂融合后延迟、受阻甚至逆转，导致交配减少。这些结果表明，Fig2将接触部位指定为降解细胞壁的“安全”位点。
