| Species | Disruptability | Reference | Submitter | |
|---|---|---|---|---|
| P. berghei ANKA |
Refractory |
RMgm-556 | Imported from RMgmDB | |
| P. berghei ANKA |
Possible |
RMgm-4845 | Imported from RMgmDB | |
| P. falciparum 3D7 |
Possible |
22127061 | Theo Sanderson, Wellcome Trust Sanger Institute | |
| P. falciparum 3D7 |
Refractory |
USF piggyBac screen (Insert. mut.) | USF PiggyBac Screen | |
| P. falciparum 3D7 |
Possible |
36154191 \'In contrast to previous findings, we showed that gene deletion Pfcrk5- parasites grew normally as asexual stages and underwent normal gametocytogenesis to stage V gametocytes. However, Pfcrk5- parasites showed a severe defect in male gametogenesis, which was evident by a significant reduction in the emergence of male gametes (exflagellation). This defect caused a severe reduction of parasite transmission to the mosquito. Genetic crosses performed using sex-specific sterile transgenic parasites revealed that Pfcrk5- parasites suffered a defect in male fertility but female gametes were fertile. Taken together, these results demonstrate that PfCRK5 is a critical sexual stage kinase which regulates male gametogenesis and transmission to the mosquito.\' |
Theo Sanderson, Francis Crick Institute | |
| Species | Stage | Phenotype | Reference | Submitter |
|---|---|---|---|---|
| P. berghei ANKA | Asexual |
No difference |
RMgm-4845 | Imported from RMgmDB |
| P. falciparum 3D7 | Asexual |
No difference |
36154191 \'In contrast to previous findings, we showed that gene deletion Pfcrk5- parasites grew normally as asexual stages and underwent normal gametocytogenesis to stage V gametocytes. However, Pfcrk5- parasites showed a severe defect in male gametogenesis, which was evident by a significant reduction in the emergence of male gametes (exflagellation). This defect caused a severe reduction of parasite transmission to the mosquito. Genetic crosses performed using sex-specific sterile transgenic parasites revealed that Pfcrk5- parasites suffered a defect in male fertility but female gametes were fertile. Taken together, these results demonstrate that PfCRK5 is a critical sexual stage kinase which regulates male gametogenesis and transmission to the mosquito.\' |
Theo Sanderson, Francis Crick Institute |
| P. berghei ANKA | Gametocyte |
Difference from wild-type |
RMgm-4845
Normal gametocyte production. Only a few microgametocytes formed active exflagellation centres after activation. |
Imported from RMgmDB |
| P. falciparum 3D7 | Gametocyte |
Attenuated |
36154191 \'In contrast to previous findings, we showed that gene deletion Pfcrk5- parasites grew normally as asexual stages and underwent normal gametocytogenesis to stage V gametocytes. However, Pfcrk5- parasites showed a severe defect in male gametogenesis, which was evident by a significant reduction in the emergence of male gametes (exflagellation). This defect caused a severe reduction of parasite transmission to the mosquito. Genetic crosses performed using sex-specific sterile transgenic parasites revealed that Pfcrk5- parasites suffered a defect in male fertility but female gametes were fertile. Taken together, these results demonstrate that PfCRK5 is a critical sexual stage kinase which regulates male gametogenesis and transmission to the mosquito.\' |
Theo Sanderson, Francis Crick Institute |
| P. berghei ANKA | Ookinete |
Difference from wild-type |
RMgm-4845
CRK5-KO parasites showed a significant reduction in ookinete conversion compared to the parental control line |
Imported from RMgmDB |
| P. berghei ANKA | Oocyst |
Difference from wild-type |
RMgm-4845
A > 30 fold decrease in the number of CRK5-KO oocysts present oin A. stephensi mosquitoes allowed to feed on infected mice. Oocysts showed aberrant morphology. No formation of viable sporozoites. No blood stage infection developed in mice after infection by bite of infected mosquitoes. |
Imported from RMgmDB |
| P. berghei ANKA | Sporozoite |
Difference from wild-type |
RMgm-4845
A > 30 fold decrease in the number of CRK5-KO oocysts present in A. stephensi mosquitoes allowed to feed on infected mice. Oocysts showed aberrant morphology. No formation of viable sporozoites. No blood stage infection developed in mice after infection by bite of infected mosquitoes. |
Imported from RMgmDB |
| P. berghei ANKA | Liver |
Difference from wild-type |
RMgm-4845
A > 30 fold decrease in the number of CRK5-KO oocysts present in A. stephensi mosquitoes allowed to feed on infected mice. Oocysts showed aberrant morphology. No formation of viable sporozoites. No blood stage infection developed in mice after infection by bite of infected mosquitoes. |
Imported from RMgmDB |
| PlasmoDB | PKNH_1134500 |
| GeneDB | PKNH_1134500 |
| Malaria Metabolic Pathways | Localisation images Pathways mapped to |
| Previous ID(s) | PK6_1350w, PKH_113350 |
| Orthologs | PBANKA_1230200 , PCHAS_1230900 , PF3D7_0615500 , PVP01_1133600 , PVX_113910 , PY17X_1233700 |
| Google Scholar | Search for all mentions of this gene |