Successful modification | The parasite was generated by the genetic modification |
The mutant contains the following genetic modification(s) |
Gene disruption
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Reference (PubMed-PMID number) |
Reference 1 (PMID number) : 29253313 |
MR4 number |
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Parent parasite used to introduce the genetic modification |
Rodent Malaria Parasite | P. yoelii |
Parent strain/line | P. y. yoelii 17XNL |
Name parent line/clone |
Not applicable
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Other information parent line | |
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The mutant parasite was generated by |
Name PI/Researcher | Steel RWJ, Kappe SHI |
Name Group/Department | Center for Infectious Disease Research |
Name Institute | formerly Seattle Biomedical Research Institute |
City | Seattle |
Country | USA |
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Name of the mutant parasite |
RMgm number | RMgm-4406 |
Principal name | plp1/spect2(-) |
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 | Not different from wild type |
Oocyst | Not different from wild type |
Sporozoite | Normal numbers of salivary gland sporozoites. Injection of 100 sporozoites revealed that Py plp1/spect2¯ sporozoites were significantly less infectious than Py WT sporozoites (1 out of 10 mice developed blood stage parasitemia). When infection was delivered by five mosquito bites, all Py WT infected mice but none of the Py plp1/spect2¯ infected mice developed blood stage infection. Increasing the challenge to 15 infectious bites resulted in 7% of Py plp1/spect2¯ infected mice developing blood stage infection, with a greater than one-day delay to patency observed for infected mice of both groups compared to Py WT. Reduced hepatocyte cell traversal in vitro. Normal/higher hepatocyte invasion rate in vitro compared to wild type. |
Liver stage | Injection of 100 sporozoites revealed that Py plp1/spect2¯ sporozoites were significantly less infectious than Py WT sporozoites (1 out of 10 mice developed blood stage parasitemia). When infection was delivered by five mosquito bites, all Py WT infected mice but none of the Py plp1/spect2¯ infected mice developed blood stage infection. Increasing the challenge to 15 infectious bites resulted in 7% of Py plp1/spect2¯ infected mice developing blood stage infection, with a greater than one-day delay to patency observed for infected mice of both groups compared to Py WT. Reduced hepatocyte cell traversal in vitro. Normal/higher hepatocyte invasion rate in vitro compared to wild type. |
Additional remarks phenotype | Mutant/mutation
The mutant lacks expression of plp1 (spect2).
Protein (function)
The spect2/pplp1 gene is a member of a small, conserved family of proteins encoding perforin-like proteins containing membrane-attack complex/perforin domains (MACPF). The P. yoelii genome contains 5 PLP proteins
Phenotype
Normal numbers of salivary gland sporozoites. Injection of 100 sporozoites revealed that Py plp1/spect2¯ sporozoites were significantly less infectious than Py WT sporozoites (1 out of 10 mice developed blood stage parasitemia). When infection was delivered by five mosquito bites, all Py WT infected mice but none of the Py plp1/spect2¯ infected mice developed blood stage infection. Increasing the challenge to 15 infectious bites resulted in 7% of Py plp1/spect2¯ infected mice developing blood stage infection, with a greater than one-day delay to patency observed for infected mice of both groups compared to Py WT. Reduced hepatocyte cell traversal in vitro. Normal/higher hepatocyte invasion rate in vitro compared to wild type.
Additional information
Other mutants |