A Plasmodium homolog of ER tubule-forming proteins is required for parasite virulence |
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| Authors: | Xiaoyu Shi Lei Hai Kavitha Govindasamy Jian Gao Isabelle Coppens Junjie Hu Qian Wang Purnima Bhanot |
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| Institution: | 1. Department of Immunology, School of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, Tianjin Medical University, Tianjin, China;2. Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ, USA;3. Department of Molecular Microbiology and Immunology, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA;4. National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China |
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| Abstract: | 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. |
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| Keywords: | DP1 endoplasmic reticulum REEP reticulon YOP1 |
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