Institute of Parasitology and Centre for Host-Parasite Interactions, McGill University, 21,111 Lakeshore Road, Sainte-Anne-de-Bellevue, Que. H9X3V9, Canada.
Int J Parasitol. 2010 Jul;40(8):979-88. doi: 10.1016/j.ijpara.2010.02.010. Epub 2010 Mar 12.
The completion of the Plasmodium (malaria) life cycle in the mosquito requires the parasite to traverse first the midgut and later the salivary gland epithelium. We have identified a putative kinase-related protein (PKRP) that is predicted to be an atypical protein kinase, which is conserved across many species of Plasmodium. The pkrp gene encodes a RNA of about 5300 nucleotides that is expressed as a 90kDa protein in sporozoites. Targeted disruption of the pkrp gene in Plasmodium berghei, a rodent model of malaria, compromises the ability of parasites to infect different tissues within the mosquito host. Early infection of mosquito midgut is reduced by 58-71%, midgut oocyst production is reduced by 50-90% and those sporozoites that are produced are defective in their ability to invade mosquito salivary glands. Midgut sporozoites are not morphologically different from wild-type parasites by electron microscopy. Some sporozoites that emerged from oocysts were attached to the salivary glands but most were found circulating in the mosquito hemocoel. Our findings indicate that a signalling pathway involving PbPKRP regulates the level of Plasmodium infection in the mosquito midgut and salivary glands.
疟原虫(疟疾)在蚊子体内完成生命周期需要寄生虫首先穿越中肠,然后穿越唾液腺上皮。我们已经鉴定出一种假定的激酶相关蛋白(PKRP),它被预测为一种非典型的蛋白激酶,在许多疟原虫物种中都保守。pkrp 基因编码约 5300 个核苷酸的 RNA,在孢子虫中表达为 90kDa 的蛋白质。在疟原虫伯氏疟原虫(一种疟疾的啮齿动物模型)中靶向破坏 pkrp 基因,会损害寄生虫感染蚊子宿主内不同组织的能力。蚊子中肠的早期感染减少了 58-71%,中肠卵囊的产生减少了 50-90%,并且产生的那些孢子虫在入侵蚊子唾液腺的能力上存在缺陷。电子显微镜下,中肠孢子虫在形态上与野生型寄生虫没有区别。一些从卵囊中出现的孢子虫附着在唾液腺上,但大多数在蚊子血腔中循环。我们的发现表明,涉及 PbPKRP 的信号通路调节疟原虫在蚊子中肠和唾液腺中的感染水平。