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人类致病酵母白色念珠菌的过氧化氢酶基因破坏株在菌丝生长方面存在缺陷,并且一种过氧化氢酶特异性抑制剂能够抑制野生型细胞的菌丝生长。

Catalase gene disruptant of the human pathogenic yeast Candida albicans is defective in hyphal growth, and a catalase-specific inhibitor can suppress hyphal growth of wild-type cells.

作者信息

Nakagawa Yoshiyuki

机构信息

Division of Molecular Mycology and Medicine, Center for Neurological Disease and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.

出版信息

Microbiol Immunol. 2008 Jan;52(1):16-24. doi: 10.1111/j.1348-0421.2008.00006.x.

Abstract

Although the catalase gene (CAT1) disruptant of the human pathogenic yeast Candida albicans was viable under ordinary growth conditions, we previously found that it could not grow on YPD (yeast extract/peptone/dextrose) containing SDS or at higher growth temperatures. To investigate the pleiotrophic nature of the disruptant, we examined the effect of the catalase inhibitor 3-AT on the growth of wild-type strains. Surprisingly, the addition of 3-AT and SDS caused the wild-type cells to be non-viable on YPD plates. We found an additional phenotype of the catalase gene disruptant: it did not produce normal hyphae on Spider medium. Hyphal growth was observed in a CAP1 (Candida AP-1-like protein gene) disruptant, a HOG1 (high-osmolarity glycerol signaling pathway gene) disruptant, and the double CAP1/HOG1 disruptant, suggesting that the defect in hyphal formation by the catalase disruptant was independent of these genes. Addition of 3-AT and SDS to hyphae-inducing media suppressed growth of normal hyphae in the wild-type strain. The potential necessity for catalase action upon exposure to hyphae-inducing conditions was confirmed by the immediate elevation of the catalase gene message. In spite of the requirement for catalase during hyphal growth, the catalase gene disruptant was capable of forming germ tubes in medium containing serum.

摘要

尽管人类致病酵母白色念珠菌的过氧化氢酶基因(CAT1)缺失突变体在正常生长条件下能够存活,但我们之前发现它无法在含有SDS的YPD(酵母提取物/蛋白胨/葡萄糖)培养基上生长,也不能在较高生长温度下生长。为了研究该缺失突变体的多效性,我们检测了过氧化氢酶抑制剂3-AT对野生型菌株生长的影响。令人惊讶的是,添加3-AT和SDS会导致野生型细胞在YPD平板上无法存活。我们发现了过氧化氢酶基因缺失突变体的另一个表型:它在蜘蛛培养基上不能产生正常的菌丝。在CAP1(白色念珠菌AP-1样蛋白基因)缺失突变体、HOG1(高渗甘油信号通路基因)缺失突变体以及双CAP1/HOG1缺失突变体中观察到了菌丝生长,这表明过氧化氢酶缺失突变体在菌丝形成方面的缺陷与这些基因无关。向菌丝诱导培养基中添加3-AT和SDS会抑制野生型菌株中正常菌丝的生长。过氧化氢酶基因信息的立即升高证实了在暴露于菌丝诱导条件下过氧化氢酶作用的潜在必要性。尽管在菌丝生长过程中需要过氧化氢酶,但过氧化氢酶基因缺失突变体能够在含有血清的培养基中形成芽管。

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