A Plasmodium homolog of ER tubule-forming proteins is required for parasite virulence.
Xiaoyu ShiLei HaiKavitha GovindasamyJian GaoIsabelle CoppensJunjie HuQian WangPurnima BhanotPublished in: Molecular microbiology (2020)
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.
Keyphrases
- plasmodium falciparum
- endoplasmic reticulum
- estrogen receptor
- breast cancer cells
- induced apoptosis
- escherichia coli
- staphylococcus aureus
- risk factors
- gene expression
- genome wide
- subarachnoid hemorrhage
- dna methylation
- adipose tissue
- copy number
- cell cycle arrest
- cell death
- cell proliferation
- brain injury
- transcription factor
- biofilm formation
- blood brain barrier
- toxoplasma gondii