The genome of Cryptosporidium hominis

The genome of Cryptosporidium hominis
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DOI:
10.1038/nature02977
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发表时间:
2004-10-28
期刊:
影响因子:
64.8
通讯作者:
Buck, GA
Buck, GA
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Xu, P;Widmer, G;Buck, GA

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隐孢子虫在世界范围内引起急性胃肠炎和腹泻。它们是顶复门(Apicomplexa)的成员,顶复门是原生动物病原体,通过使用专门的顶端复合体侵入宿主细胞,通常通过无脊椎动物载体或中间宿主传播。与其他顶复门不同,隐孢子虫通过摄取卵囊传播,并在单一宿主中完成其生命周期。没有可用的治疗方法,控制重点是消除供水中的卵囊(1)。2种,C. hominis和C.在宿主范围、基因型和致病性方面不同的细小病毒与人类最相关(1-3)。C. hominis仅限于人类,而C.小孢子虫也感染其他哺乳动物(2)。本文描述了一个与920万碱基的C.人(2)。C.人的蛋白质编码基因显示出与寄生虫栖息的环境小生境所施加的要求惊人的一致性。能量代谢主要来自糖酵解。有氧代谢和无氧代谢都是可行的,前者需要一个简化的电子传递系统。生物合成能力是有限的,解释了广泛的运输。没有顶质体的证据,但存在与顶端复杂细胞器相关的基因。C. hominis和C.寄生虫表现出非常相似的基因互补,这些寄生虫之间的表型差异一定是由于细微的序列差异。
Cryptosporidium species cause acute gastroenteritis and diarrhoea worldwide. They are members of the Apicomplexa - protozoan pathogens that invade host cells by using a specialized apical complex and are usually transmitted by an invertebrate vector or intermediate host. In contrast to other Apicomplexans, Cryptosporidium is transmitted by ingestion of oocysts and completes its life cycle in a single host. No therapy is available, and control focuses on eliminating oocysts in water supplies(1). Two species, C. hominis and C. parvum, which differ in host range, genotype and pathogenicity, are most relevant to humans(1-3). C. hominis is restricted to humans, whereas C. parvum also infects other mammals(2). Here we describe the eight-chromosome similar to9.2-million-base genome of C. hominis(2). The complement of C. hominis protein-coding genes shows a striking concordance with the requirements imposed by the environmental niches the parasite inhabits. Energy metabolism is largely from glycolysis. Both aerobic and anaerobic metabolisms are available, the former requiring an alternative electron transport system in a simplified mitochondrion. Biosynthesis capabilities are limited, explaining an extensive array of transporters. Evidence of an apicoplast is absent, but genes associated with apical complex organelles are present. C. hominis and C. parvum exhibit very similar gene complements, and phenotypic differences between these parasites must be due to subtle sequence divergence.