| 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) : 17253978
|
| 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 |
P. berghei ANKA cl15cy1
|
| Other information parent line | A reference wild type clone from the ANKA strain of P. berghei (PubMed: PMID: 17406255). |
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| The mutant parasite was generated by |
| Name PI/Researcher | J. Thompson; C.J. Janse; A.P. Waters |
| Name Group/Department | Institute of Immunology and Infection Research |
| Name Institute | School of Biological Sciences |
| City | Edinburgh |
| Country | United Kingdom |
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| Name of the mutant parasite |
| RMgm number | RMgm-199 |
| Principal name | 223cl1; 298cl1 |
| Alternative name | crmp2- |
| Standardized name | |
| Is the mutant parasite cloned after genetic modification | Yes |
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| Phenotype |
| Asexual blood stage | Not different from wild type |
| Gametocyte/Gamete | Not different from wild type |
| Fertilization and ookinete | Not different from wild type |
| Oocyst | Normal numbers of oocysts are produced. Normal numbers of oocyst-derived (hemolymph) sporozoites are formed. Sporozoites do not invade the salivary gland. |
| Sporozoite | Normal numbers of oocysts are produced. Normal numbers of oocyst-derived (hemolymph) sporozoites are formed. Sporozoites do not invade the salivary gland. Sporozoites do not transmit to the mouse by infected mosquito bite. Intravenous inoculation of sporozoites results in blood stage infections, although at a lower efficiency compared to wild type sporozoites. |
| Liver stage | Sporozoites do not invade the salivary gland. Sporozoites do not transmit to the mouse by infected mosquito bite. Intravenous inoculation of sporozoites results in blood stage infections, although at a lower efficiency compared to wild type sporozoites. |
| Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of Cysteine Repeat Modular Proteins (CRMP2)
Protein (function)
The Cysteine Repeat Modular Proteins (CRMP1–4) of Plasmodium, are encoded by a small gene family that is conserved in malaria and other Apicomplexan parasites. They are very large, predicted surface proteins with multipass transmembrane domains containing motifs that are conserved within families of cysteine-rich, predicted surface proteins in a range of unicellular eukaryotes, and a unique combination of protein-binding motifs, including a > 100 kDa cysteine-rich modular region, an epidermal growth factor-like domain and a Kringle domain.
Phenotype
The phenotype analyses indicate that CRMP2 is not essential for blood stage development and for the formation of sporozoites. CRMP2 is essential for sporozoite targeting into the mosquito salivary gland and therefore for transmission of the parasite from the mosquito to the mouse.
Additional information
CRMP2 is expressed both in asexual blood stages and in oocysts and sporozoites. Evidence has been presented for a location on the erythrocyte membrane of schizont infected red blood cells sporozoites. No evidence was found for an effect on blood stage development as a result of the lack of expression of CRMP2 in the blood stages. The growth of mutant parasites in mice was comparable to wild type parasites. It has been suggested that domains of this protein may play a role in immune regulation by binding to host immune molecules and thereby modifying the course of the immune response.
Two gene models exist: PB000158.02.0 and PB001595.02.0
Other mutants
RMgm-198: A mutant lacking expression of CRMP1 |
*RMgm-199
