细胞生物学
效应器
生物
弓形虫
线粒体
寄生虫寄主
免疫学
抗体
计算机科学
万维网
作者
Xianhe Li,Julian Straub,Tania Medeiros,Chahat Mehra,Fabian den Brave,Esra Peker,Ilian Atanassov,Katharina Stillger,Jonas B. Michaelis,Emma Burbridge,Colin Adrain,Christian Münch,Jan Riemer,Thomas Becker,Lena Pernas
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2022-01-14
卷期号:375 (6577)
被引量:39
标识
DOI:10.1126/science.abi4343
摘要
The outer mitochondrial membrane (OMM) is essential for cellular homeostasis. Yet little is known of the mechanisms that remodel it during natural stresses. We found that large “SPOTs” (structures positive for OMM) emerge during Toxoplasma gondii infection in mammalian cells. SPOTs mediated the depletion of the OMM proteins mitofusin 1 and 2, which restrict parasite growth. The formation of SPOTs depended on the parasite effector TgMAF1 and the host mitochondrial import receptor TOM70, which is required for optimal parasite proliferation. TOM70 enabled TgMAF1 to interact with the host OMM translocase SAM50. The ablation of SAM50 or the overexpression of an OMM-targeted protein promoted OMM remodeling independently of infection. Thus, Toxoplasma hijacks the formation of SPOTs, a cellular response to OMM stress, to promote its growth.
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