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A Plasmodium homolog of ER tubule-forming proteins is required for parasite virulence.
Molecular Microbiology ( IF 2.6 ) Pub Date : 2020-05-20 , DOI: 10.1111/mmi.14526 Xiaoyu Shi 1 , Lei Hai 1 , Kavitha Govindasamy 2 , Jian Gao 1 , Isabelle Coppens 3 , Junjie Hu 4 , Qian Wang 1, 4 , Purnima Bhanot 2
Molecular Microbiology ( IF 2.6 ) Pub Date : 2020-05-20 , DOI: 10.1111/mmi.14526 Xiaoyu Shi 1 , Lei Hai 1 , Kavitha Govindasamy 2 , Jian Gao 1 , Isabelle Coppens 3 , Junjie Hu 4 , Qian Wang 1, 4 , Purnima Bhanot 2
Affiliation
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Reticulon and REEP family of proteins stabilize the high curvature of endoplasmic reticulum (ER) tubules. Plasmodium berghei Yop1 (PbYop1) is a REEP5 homolog in Plasmodium. Here, we characterize its function using a gene‐knockout (Pbyop1∆). Pbyop1∆ asexual stage parasites display abnormal ER architecture and an enlarged digestive vacuole. The erythrocytic cycle of Pbyop1∆ parasites is severely attenuated and the incidence of experimental cerebral malaria is significantly decreased in Pbyop1∆‐infected mice. Pbyop1∆ sporozoites have reduced speed, are slower to invade host cells but give rise to equal numbers of infected HepG2 cells, as WT sporozoites. We propose that PbYOP1’s disruption may lead to defects in trafficking and secretion of a subset of proteins required for parasite development and invasion of erythrocytes. Furthermore, the maintenance of ER morphology in different parasite stages is likely to depend on different proteins.
中文翻译：
寄生虫毒力需要ER小管形成蛋白的疟原虫同源物。
网状蛋白和REEP蛋白家族可稳定内质网（ER）小管的高曲率。伯氏疟原虫Yop1（Pb Yop1）是疟原虫中的REEP5同源物。在这里，我们使用基因敲除（Pb yop1∆）表征其功能。Pb yop1∆无性寄生虫显示异常的ER结构和扩大的消化液。的红细胞周期的Pb yop1Δ寄生虫被严重衰减，并且实验性脑疟疾的发病率中显著降低铅yop1Δ感染的小鼠。铅含量yop1∆子孢子的速度降低，入侵宿主细胞的速度较慢，但与WT子孢子一样，感染的HepG2细胞数量也相同。我们认为Pb YOP1的破坏可能导致寄生虫发育和入侵红细胞所需的一部分蛋白质的运输和分泌缺陷。此外，在不同的寄生虫阶段中，ER形态的维持可能取决于不同的蛋白质。
更新日期：2020-05-20
中文翻译：
寄生虫毒力需要ER小管形成蛋白的疟原虫同源物。
网状蛋白和REEP蛋白家族可稳定内质网（ER）小管的高曲率。伯氏疟原虫Yop1（Pb Yop1）是疟原虫中的REEP5同源物。在这里，我们使用基因敲除（Pb yop1∆）表征其功能。Pb yop1∆无性寄生虫显示异常的ER结构和扩大的消化液。的红细胞周期的Pb yop1Δ寄生虫被严重衰减，并且实验性脑疟疾的发病率中显著降低铅yop1Δ感染的小鼠。铅含量yop1∆子孢子的速度降低，入侵宿主细胞的速度较慢，但与WT子孢子一样，感染的HepG2细胞数量也相同。我们认为Pb YOP1的破坏可能导致寄生虫发育和入侵红细胞所需的一部分蛋白质的运输和分泌缺陷。此外，在不同的寄生虫阶段中，ER形态的维持可能取决于不同的蛋白质。
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