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A Plasmodium homolog of ER tubule‐forming proteins is required for parasite virulence
Author(s) -
Shi Xiaoyu,
Hai Lei,
Govindasamy Kavitha,
Gao Jian,
Coppens Isabelle,
Hu Junjie,
Wang Qian,
Bhanot Purnima
Publication year - 2020
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.14526
Subject(s) - biology , endoplasmic reticulum , plasmodium berghei , plasmodium (life cycle) , parasite hosting , virulence , microbiology and biotechnology , secretion , vacuole , gene , malaria , cytoplasm , immunology , genetics , biochemistry , world wide web , computer science
Reticulon and REEP family of proteins stabilize the high curvature of endoplasmic reticulum (ER) tubules. Plasmodium berghei Yop1 ( Pb Yop1) is a REEP5 homolog in Plasmodium . Here, we characterize its function using a gene‐knockout ( Pb yop1∆). Pb yop1∆ asexual stage parasites display abnormal ER architecture and an enlarged digestive vacuole. The erythrocytic cycle of Pb yop1∆ parasites is severely attenuated and the incidence of experimental cerebral malaria is significantly decreased in Pb yop1∆‐infected mice. Pb yop1∆ 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 Pb YOP1’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.