| 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) : 18848846
|
| 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 | C. Lavazec, G.R. Mair, C.J. Janse, J. Templeton |
| Name Group/Department | Department of Microbiology and Immunology |
| Name Institute | Weill Cornell Medical College |
| City | New York |
| Country | USA |
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| Name of the mutant parasite |
| RMgm number | RMgm-121 |
| Principal name | ∆PbCCp1 |
| Alternative name | 429cl1 |
| 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. Sporozoite formation within the oocysts is blocked. Analysis of the morphology of oocysts by light microscopy revealed that the majority of 17–22 day oocysts were either vacuolated or non-sporulated, and did not contain sporozoites. |
| Sporozoite | No hemocoel and salivary gland sporozoites were detected. |
| Liver stage | Not tested |
| Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of CCp1 (LAP2, LCCL/lectin adhesive-like protein 2; LCCL domain containing protein CCp1).
Protein (function)
The ccp1 gene is a member of a small conserved gene family, encoding proteins with multiple adhesive domains, for example a Lgl1 (LCCL)-lectin adhesive domain. In P. falciparum the LCCL domain-containing proteins are termed PfCCp's and in P. berghei PbLAP's.
Phenotype
Phenotype analyses indicate a role during oocyst development and sporozoite formation/production (see also additional information).
Additional information
In another study (Raine, J.D. et al., 2007, PloS Pathogens 3, e30) it has been shown that crossings of ∆lap2 (ccp1) mutant females with wild type males did not rescue the formation of sporozoites. In contrast, crossing of the mutant males with wild type females resulted in wild type production of sporozoites that were infectious to C57BL/6 mice.
The lack of rescue of the ∆lap2 (ccp1) mutant phenotype by crossing of mutant females with wild type males is suggestive of a role of LAP2 (CCp1) within a few hours after fertilisation.
Other members of the LAP/CCp family of proteins have been analysed by targeted gene disruption. A number of mutants lacking expression of these proteins show a comparable defect in development of oocysts and formation of sporozoites (RMgm-113, RMgm-114, RMgm-115: LAP1/PbSLAP/PbSR/CCp3; RMgm-119: LAP4/CCp2; RMgm-98: LAP5/FNPA; RMgm-120: LAP6, CCp4).
Other mutants
RMgm-118: An independent mutant lacking expression of LAP2/CCp1
RMgm-124: A mutant lacking expression of both LAP2/CCP1 and PbSR/PSLAP/LAP1/CCp3
RMgm-125: A mutant lacking expression of both LAP2/CCP1 and LAP6/CCp4 |
*RMgm-121
