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疟原虫的雄性生育能力由一种植物型繁殖因子GCS1决定。

Male fertility of malaria parasites is determined by GCS1, a plant-type reproduction factor.

作者信息

Hirai Makoto, Arai Meiji, Mori Toshiyuki, Miyagishima Shin-Ya, Kawai Satoru, Kita Kiyoshi, Kuroiwa Tsuneyoshi, Terenius Olle, Matsuoka Hiroyuki

机构信息

Division of Medical Zoology, Department of Infection and Immunity, Jichi Medical University School of Medicine, Shimotsuke City, Tochigi 329-0498, Japan.

出版信息

Curr Biol. 2008 Apr 22;18(8):607-13. doi: 10.1016/j.cub.2008.03.045. Epub 2008 Apr 10.

Abstract

Malaria, which is caused by Plasmodium parasites, is transmitted by anopheline mosquitoes. When gametocytes, the precursor cells of Plasmodium gametes, are transferred to a mosquito, they fertilize and proliferate, which render the mosquito infectious to the next vertebrate host. Although the fertilization of malaria parasites has been considered as a rational target for transmission-blocking vaccines, the underlying mechanism is poorly understood. Here, we show that the rodent malaria parasite gene Plasmodium berghei GENERATIVE CELL SPECIFIC 1 (PbGCS1) plays a central role in its gametic interaction. PbGCS1 knockout parasites show male sterility, resulting in unsuccessful fertilization. Because such a male-specific function of GCS1 has been observed in angiosperms, this indicates, for the first time, that parasite sexual reproduction is controlled by a machinery common to flowering plants. Our present findings provide a new viewpoint for understanding the parasitic fertilization system and important clues for novel strategies to attack life-threatening parasites.

摘要

疟疾由疟原虫寄生虫引起,通过按蚊传播。当疟原虫配子的前体细胞即配子体被转移到蚊子体内时,它们会受精并增殖,从而使蚊子能够感染下一个脊椎动物宿主。尽管疟原虫的受精被认为是传播阻断疫苗的合理靶点,但其潜在机制却知之甚少。在此,我们表明啮齿动物疟原虫基因伯氏疟原虫生殖细胞特异性1(PbGCS1)在其配子相互作用中起核心作用。PbGCS1基因敲除的寄生虫表现出雄性不育,导致受精失败。由于在被子植物中已观察到GCS1的这种雄性特异性功能,这首次表明寄生虫的有性生殖受开花植物共有的机制控制。我们目前的研究结果为理解寄生虫受精系统提供了新的视角,并为攻击危及生命的寄生虫的新策略提供了重要线索。

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