Cryptosporidium parvum appears to lack a plastid genome
Cryptosporidium parvum appears to lack a plastid genome
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DOI：
10.1099/00221287-146-2-315
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发表时间：
2000-02-01
期刊：
影响因子：
2.8
通讯作者：
Keithly, JS
中科院分区：
文献类型：
--
作者：
Zhu, G;Marchewka, MJ;Keithly, JS
令人惊讶的是，与大多数顶复虫不同，细小隐孢子虫似乎缺乏质体基因组，基于高度保守的质体小或大亚基rRNA （SSU/LSU rRNA）和其他顶复虫门成员的tUfA-tRNA（Phe）基因的引物无法扩增出细小隐孢子虫胞内阶段的产物。而从含质体的顶复合体牛艾美耳虫和刚地弓形虫，以及植物葱和菠菜中获得的产物。孢子子基因组DNA （gDNA）的斑点杂交支持了这些PCR结果，一组含有SSU/LSU rRNA和tufA-tRNA（Phe）基因的弓形虫质体特异性探针与含有不同质体的生物（包括三种顶复合体、两种植物和细叶藻）的gDNA强烈杂交，但与没有这种细胞器的生物（包括C. parvum、三种动质体、酵母、酿酒酵母、哺乳动物和大肠杆菌）的gDNA不杂交。由于质体在其他顶复合体中的起源被认为是红藻或绿藻次生共生的结果，因此对其在小弧菌中缺失的最简洁的解释是它是次生丢失的。如果得到证实，这将表明该细胞器在顶复合体的一个成员中有另一种进化命运，这也表明与由顶复合体成员引起的其他疾病不同，针对与隐孢子虫病相关的质体基因组或代谢途径的药物开发可能并不有用。
Surprisingly, unlike most Apicomplexa, Cryptosporidium parvum appears to lack a plastid genome, Primers based upon the highly conserved plastid small-or large-subunit rRNA (SSU/LSU rRNA) and the tUfA-tRNA(Phe) genes of other members of the phylum Apicomplexa failed to amplify products from intracellular stages of C. parvum. whereas products were obtained from the plastid-containing apicomplexans Eimeria bovis and Toxoplasma gondii, as well as the plants Allium stellatum and Spinacia oleracea. Dot-blot hybridization of sporozoite genomic DNA (gDNA) supported these PCR results, A T, gondii plastid-specific set of probes containing SSU/LSU rRNA and tufA-tRNA(Phe) genes strongly hybridized to gDNA from a diverse group of plastid-containing organisms including three Apicomplexa, two plants, and Euglena gracilis, but not to those without this organelle including C. parvum, three kinetoplastids, the yeast Saccharomyces cerevisiae, mammals and the eubacterium Escherichia coli, Since the origin of the plastid in other apicomplexans is postulated to be the result of a secondary symbiogenesis of either a red or a green alga, the most parsimonious explanation for its absence in C. parvum is that it has been secondarily lost, If confirmed, this would indicate an alternative evolutionary fate for this organelle in one member of the Apicomplexa, It also suggests that unlike the situation with other diseases caused by members of the Apicomplexa, drug development against cryptosporidiosis targeting a plastid genome or metabolic pathways associated with it may not be useful.