| 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) : 18434537
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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 |
P. berghei ANKA 2.34
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| Other information parent line | P. berghei ANKA 2.34 is a cloned, gametocyte producer line of the ANKA strain (PubMed: PMID: 15137943). |
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| The mutant parasite was generated by |
| Name PI/Researcher | P. Ellekvist; N. Kumar |
| Name Group/Department | Department of Cellular and Molecular Medicine, Faculty of Health Sciences |
| Name Institute | University of Copenhagen |
| City | Copenhagen |
| Country | Denmark |
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| Name of the mutant parasite |
| RMgm number | RMgm-230 |
| Principal name | kch1-null |
| Alternative name | |
| Standardized name | |
| Is the mutant parasite cloned after genetic modification | Yes |
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| Phenotype |
| Asexual blood stage | Mice infected with mutant parasites rapidly progressed in parasitaemia from day 4. In contrast to wild type-infected mice, however, parasitaemia in mutant-infected mice leveled off at a plateau 9 days after infection, before approaching the parasitaemia of wild type-infected mice at day 14. This delay in parasitaemia was not statistically significant. Mutant-infected mice showed a slightly prolonged survival compared with wild type-infected mice. |
| Gametocyte/Gamete | Normal gametocyte production |
| Fertilization and ookinete | Normal ookinete production. |
| Oocyst | Mosquitoes infected (81 of 89 dissected) with wild type parasites revealed a median oocyst number of 115 per mosquito (25 and 75 percentiles, oocyst numbers 37 and 251). Only two mosquitoes of 112 fed on mutant-infected mice had oocysts in their midguts, thus demonstrating a 98% reduction in the infectivity of mutant parasites during transmission through mosquitoes. |
| Sporozoite | Not different from wild type |
| Liver stage | Not different from wild type |
| Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of Kch1(K+ channel, potassium channel)
Protein (function)
K+ channels constitute the largest and most diverse of ion channel families and are involved in K+ transport, cell volume control, and regulation of membrane potential. Two putative K+ channel-encoding genes have been found in the P. falciparum genome
Phenotype
Physiological and functional studies with the mutant parasites suggest that Kch1 mediates K+ uptake in the blood stages. The phenotype analyses show that Kch1 is not essential for the blood stages. However, it is critical for the development of the mosquito midgut oocyst stage of the parasite.
Additional information
A marked reduction in the uptake of the K+ congener 86Rb+ was demonstrated in the blood stages of the mutant parasites.
Other mutants |
*RMgm-230
