Mutational analysis of the glycosylphosphatidylinositol (GPI) anchor pathway demonstrates that GPI-anchored proteins are required for cell wall biogenesis and normal hyphal growth in Neurospora crassa
Mutational analysis of the glycosylphosphatidylinositol (GPI) anchor pathway demonstrates that GPI-anchored proteins are required for cell wall biogenesis and normal hyphal growth in Neurospora crassa
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DOI：
10.1128/ec.5.3.587-600.2006
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发表时间：
2006-03-01
期刊：
影响因子：
--
通讯作者：
Free, SJ
中科院分区：
文献类型：
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作者：
Bowman, SM;Piwowar, A;Free, SJ
使用突变和蛋白质组学方法，我们证明了糖基磷脂酰肌醇（GPI）锚定途径对于细胞壁合成和完整性以及丝状真菌粗糙脉孢菌整体形态的重要性。受 gpig-1、gpip-1、gpip-2、gpip-3 和 gpit-1 基因影响的突变体已被表征，这些基因编码粗糙链孢菌 GPI 锚定生物合成途径的成分。 GPI锚定突变体表现出菌落形态、生长速率显着降低、菌丝生长模式改变、大量细胞裂解以及异常的“细胞内细胞”表型。突变体在 GPI 锚定蛋白的产生方面存在缺陷，验证了每个改变的基因对 GPI 锚定过程的需求。突变细胞壁异常脆弱，蛋白质含量减少，碳水化合物组成也发生改变。突变细胞壁缺乏许多 GPI 锚定蛋白，推测这些蛋白参与细胞壁生物发生和重塑。从这些研究中，我们得出结论，GPI 锚定通路对于粗糙脉孢菌细胞壁的正常结构和功能至关重要。
Using mutational and proteomic approaches, we have demonstrated the importance of the glycosylphosphatidylinositol (GPI) anchor pathway for cell wall synthesis and integrity and for the overall morphology of the filamentous fungus Neurospora crassa. Mutants affected in the gpig-1, gpip-1, gpip-2, gpip-3, and gpit-1 genes, which encode components of the N. crassa GPI anchor biosynthetic pathway, have been characterized. GPI anchor mutants exhibit colonial morphologies, significantly reduced rates of growth, altered hyphal growth patterns, considerable cellular lysis, and an abnormal "cell-within-a-cell" phenotype. The mutants are deficient in the production of GPI-anchored proteins, verifying the requirement of each altered gene for the process of GPI-anchoring. The mutant cell walls are abnormally weak, contain reduced amounts of protein, and have an altered carbohydrate composition. The mutant cell walls lack a number of GPI-anchored proteins, putatively involved in cell wall biogenesis and remodeling. From these studies, we conclude that the GPI anchor pathway is critical for proper cell wall structure and function in N. crassa.