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鞘脂Δ8-去饱和酶基因的破坏导致白色念珠菌形态变化延迟。

Disruption of the sphingolipid Delta8-desaturase gene causes a delay in morphological changes in Candida albicans.

作者信息

Oura Takahiro, Kajiwara Susumu

机构信息

Department of Life Science, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259-B5 Nagatsuta, Midori-ku, Yokohama, Kanagawa 266-8501, Japan.

出版信息

Microbiology (Reading). 2008 Dec;154(Pt 12):3795-3803. doi: 10.1099/mic.0.2008/018788-0.

Abstract

Ceramides and glycosylceramides, including desaturated long-chain bases, are present in most fungi as well as animals and plants. However, as the budding yeast Saccharomyces cerevisiae is not capable of desaturating long-chain bases, little is known about the physiological roles of these compounds in fungi. To investigate the necessity of desaturation of long-chain backbones in ceramides and glucosylceramides in fungal cells, we have identified and characterized a sphingolipid Delta8-desaturase (SLD) gene from the pathogenic yeast Candida albicans. Gene disruption of the C. albicans SLD homologue led to the accumulation of (E)-sphing-4-enine, a main substrate for the SLD enzyme. Introducing the Candida SLD gene homologue into these mutant cells resulted in the recovery of synthesis of (4E, 8E)-sphinga-4,8-dienine and this gene homologue was therefore identified as a Ca-SLD gene. Additionally, the sld disruptant of C. albicans had a decreased hyphal growth rate compared with the wild-type strain. These results suggest that Delta8-desaturation of long-chain bases in ceramides plays a role in the morphogenesis of C. albicans.

摘要

神经酰胺和糖基神经酰胺,包括去饱和长链碱基,存在于大多数真菌以及动植物中。然而,由于出芽酵母酿酒酵母不能使长链碱基去饱和,关于这些化合物在真菌中的生理作用知之甚少。为了研究真菌细胞中神经酰胺和葡糖神经酰胺长链主链去饱和的必要性,我们从致病性酵母白色念珠菌中鉴定并表征了一个鞘脂Δ8 - 去饱和酶(SLD)基因。白色念珠菌SLD同源物的基因破坏导致(E)-鞘氨醇-4-烯,即SLD酶的主要底物的积累。将白色念珠菌SLD基因同源物引入这些突变细胞导致(4E,8E)-鞘氨醇-4,8-二烯的合成恢复,因此该基因同源物被鉴定为Ca-SLD基因。此外,与野生型菌株相比,白色念珠菌的sld破坏株菌丝生长速率降低。这些结果表明,神经酰胺中长链碱基的Δ8 - 去饱和在白色念珠菌的形态发生中起作用。

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