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构巢曲霉sod(VI)C1突变导致细胞壁生物合成和蛋白质分泌缺陷。

Aspergillus nidulans sod(VI)C1 mutation causes defects in cell wall biogenesis and protein secretion.

作者信息

Lee Hwan Hee, Park Jeong Seok, Chae Suhn Kee, Maeng Pil Jae, Park Hee Moon

机构信息

Department of Microbiology, College of Natural Sciences, Chungnam National University, Daejeon 305-764, South Korea.

出版信息

FEMS Microbiol Lett. 2002 Mar 5;208(2):253-7. doi: 10.1111/j.1574-6968.2002.tb11090.x.

Abstract

Growth at the restrictive temperature (42 degrees C) of Aspergillus nidulans B120, carrying the conditional-lethal mutation sod(VI)C1, was partially improved by the addition of 1.0 M sorbitol to the medium. The mutant grown at 42 degrees C, with osmotic stabilizer, showed abnormal hyphal morphology, a decrease in beta-1,3-glucan synthase activity as well as cell wall sugar content, but an increase in chitin synthase activity and N-acetyl-glucosamine content. The mutation also affected the secretion of extracellular protease. The temperature-dependent osmo-sensitive phenotype of a Saccharomyces cerevisiae alpha-COP mutation can be rescued by the A. nidulans sod(VI)C(+) gene. These results indicate that the sod(VI)C1 mutation affects proper processing of secretory proteins destined for the surface of cells or beyond.

摘要

携带条件致死突变sod(VI)C1的构巢曲霉B120在限制温度(42摄氏度)下生长时,向培养基中添加1.0 M山梨醇可使其生长得到部分改善。在42摄氏度下添加渗透稳定剂培养的突变体表现出异常的菌丝形态,β-1,3-葡聚糖合酶活性以及细胞壁糖含量降低,但几丁质合酶活性和N-乙酰葡糖胺含量增加。该突变还影响细胞外蛋白酶的分泌。酿酒酵母α-COP突变的温度依赖性渗透敏感表型可被构巢曲霉sod(VI)C(+)基因拯救。这些结果表明,sod(VI)C1突变影响了 destined for the surface of cells or beyond.分泌蛋白的正确加工。 (原文中“destined for the surface of cells or beyond”表述不完整,翻译可能存在一定局限性)

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