| 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) : 26018192
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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 | Kaneko I; Yuda M |
| Name Group/Department | Department of Medical Zoology |
| Name Institute | Mie University Graduate School of Medicine |
| City | Tsu, Mie |
| Country | Japan |
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| Name of the mutant parasite |
| RMgm number | RMgm-1279 |
| Principal name | IMC1i(–) |
| Alternative name | |
| 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 | The mutants developed into ookinetes with normal conversion rates; however, nearly all of them (99.8%) displayed abnormal morphologies (only round forms) |
| Oocyst | Strongly reduced oocyst production. |
| Sporozoite | Not tested |
| Liver stage | Not tested |
| Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of IMC1i (inner membrane complex protein 1i, putative)
Protein (function)
The three motile and invasive stages (zoites) of Plasmodium species (i.e. ookinetes, sporozoites and merozoites), as well as zoites of other apicomplexan parasites, possess a similar cortical structure termed the pellicle. The pellicle is essentially made up of the plasma membrane and an underlying double membrane structure termed the inner membrane complex (IMC). Closely associated with the IMC on its cytoplasmic side is a network of intermediate filaments termed the subpellicular network (SPN), which supports the pellicular membranes and provides mechanical strength to the cell. Several members of an Apicomplexa-specific family of proteins termed IMC1 proteins have been identified as components of the SPN. Structurally related proteins from ciliates and dinoflagellate algae have since been added to this protein family renamed ‘alveolins’, which now defines the Alveolata infrakingdom. In the genus Plasmodium, the number of members of the alveolin family has risen to 12, which are encoded by conserved and syntenic genes. The alveolin family members display differential expression between the three zoite stages of the parasite, with the largest repertoires present in the ookinete and sporozoite according to proteomic studies. It has been shown in the rodent malaria species Plasmodium berghei that the disruption of individual alveolin family members expressed in sporozoites (PbIMC1a), in ookinetes (PbIMC1b) or in both these zoites (PbIMC1h) results in morphological abnormalities that are accompanied by reduced tensile strength of the zoite stages in which they are expressed. Besides roles in morphogenesis and mechanical strength, the Plasmodium alveolins are also involved in gliding motility in both ookinetes and sporozoites, most likely through interactions with components of the glideosome that are situated within the pellicular cytoplasm.
Phenotype
The successful knock-out of imc1d indicates it has no essential role during blood stage development/multiplication. The mutants developed into ookinetes with normal conversion rates; however, nearly all of them (99.8%) displayed abnormal morphologies (only round forms). Strongly reduced oocyst production.
Additional information
Other mutants
Click on IMC1 for other gene-deletion/tagging mutants targeting IMC1 proteins |
*RMgm-1279
