Superoxide dismutases in Candida albicans:: Transcriptional regulation and functional characterization of the hyphal-induced SOD5 gene
Superoxide dismutases in Candida albicans:: Transcriptional regulation and functional characterization of the hyphal-induced SOD5 gene
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DOI：
10.1091/mbc.e03-03-0179
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发表时间：
2004-02-01
影响因子：
3.3
通讯作者：
Whiteway, M
中科院分区：
文献类型：
--
作者：
Martchenko, M;Alarco, AM;Whiteway, M
超氧化物歧化酶（SOD）将超氧自由基转化为破坏性较小的过氧化氢。已知人类机会致病菌白色念珠菌在胞质溶胶中表达CuZnSOD（SOD1）和MnSOD（SOD3），在线粒体中表达MnSOD（SOD2）。我们在C.白色念珠菌基因组。SOD 5基因转录水平在C. albicans诱导SOD 5的表达。用渗透压或氧化应激攻击白色念珠菌细胞。当细胞生长在作为唯一碳源的不可发酵底物上时，SOD 5转录也增加。Rim101p的转录因子所需的所有诱导观察到的，而Efg1p转录因子是特别需要的血清调节的表达。缺失SOD 5产生了一个可行的突变株，当细胞在营养有限的条件下生长时，该突变株显示出对过氧化氢的敏感性。Sod5p是C.白色念珠菌感染的小鼠模型。然而，sod5突变株表现出与其亲本株相同的对巨噬细胞攻击的抗性，这表明毒力的丧失不是由于对巨噬细胞攻击的敏感性增加。
Superoxide dismutases (SOD) convert superoxide radicals into less damaging hydrogen peroxide. The opportunistic human pathogen Candida albicans is known to express CuZnSOD (SOD1) and MnSOD (SOD3) in the cytosol and MnSOD (SOD2) in the mitochondria. We identified three additional CuZn-containing superoxide dismutases, SOD4, SOD5, and SOD6, within the sequence of the C. albicans genome. The transcription of SOD5 was up-regulated during the yeast to hyphal transition of C. albicans, and SOD5 was induced when C. albicans cells were challenged with osmotic or with oxidative stresses. SOD5 transcription was also increased when cells were grown on nonfermentable substrates as the only carbon source. The Rim101p transcription factor was required for all inductions observed, whereas the Efg1p transcription factor was specifically needed for serum-modulated expression. Deletion of SOD5 produced a viable mutant strain that showed sensitivity to hydrogen peroxide when cells were grown in nutrient-limited conditions. Sod5p was found to be necessary for the virulence of C. albicans in a mouse model of infection. However, the sod5 mutant strain showed the same resistance to macrophage attack as its parental strain, suggesting that the loss of virulence in not due to an increased sensitivity to macrophage attack.