| Successful modification | The parasite was generated by the genetic modification |
| The mutant contains the following genetic modification(s) |
Gene disruption
|
| Reference (PubMed-PMID number) |
Reference 1 (PMID number) : 32432369
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| MR4 number |
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| Parent parasite used to introduce the genetic modification |
| Rodent Malaria Parasite | P. berghei |
| Parent strain/line | P. berghei ANKA |
| Name parent line/clone |
Not applicable
|
| Other information parent line | |
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| The mutant parasite was generated by |
| Name PI/Researcher | Shi X, Bhanot P |
| Name Group/Department | Department of Microbiology, Biochemistry and Molecular Genetics |
| Name Institute | Rutgers New Jersey Medical School |
| City | Newark, NJ |
| Country | USA |
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| Name of the mutant parasite |
| RMgm number | RMgm-4832 |
| Principal name | Pbyop1∆ |
| Alternative name | |
| Standardized name | |
| Is the mutant parasite cloned after genetic modification | Yes |
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| Phenotype |
| Asexual blood stage | Reduced growth of asexual blood stages. Pbyop1∆ parasites have a multiplication rate of approximately 7-fold over 24 h compared to 10-fold for 127 WT parasites. |
| Gametocyte/Gamete | Not tested |
| Fertilization and ookinete | Not tested |
| Oocyst | Reduced oocysts and sporozoite loads. Partially (?) explained by reduced growth of blood stages. |
| Sporozoite | Reduced oocysts and sporozoite loads. Partially (?) explained by reduced growth of blood stages. |
| Liver stage | (Some) Evidence for reduced liver stage development |
| Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of YOP1
Protein (function)
Rodent-infective and human-infective Plasmodium species encodes three homologs of proteins that induce membrane curvature and form ER tubules in higher eukaryotes, YOP1 (PF3D7_0316700 ), YOP1-like (YOP1L; PF3D7_1358700) and RTN1 (PBANKA_1139900). The primary structures of YOP1, YOP1L and RTN1 are highly conserved amongst rodent and human Plasmodium species (71-73% identity in amino acid sequence).
Phenotype
Reduced growth of asexual blood stages. Pbyop1∆ parasites have a multiplication rate of approximately 7-fold over 24 h compared to 10-fold for 127 WT parasites.
Reduced oocysts and sporozoite loads. Partially (?) explained by reduced growth of blood stages.
(Some) Evidence for reduced liver stage development.
Evidence is presented that:
- YOP1 proteins may play an evolutionarily conserved role in maintaining ER and vacuole morphology
Additional information
IFA analyses showed: In asexual stages, PbYOP1 is present in subcellular structures consistent with the peripheral ER. As observed with yeast and mammalian homologs, PbYOP1 partially co-localizes with a pan-ER marker BiP1, a protein resident in the ER lumen. In sporozoites, PbYOP1’s localization is primarily perinuclear, consistent with ER localization. PbYOP1 was not detectable in liver stages 48 h post infection
Other mutants |
*RMgm-4832
