Species | Disruptability | Reference | Submitter | |
---|---|---|---|---|
P. berghei ANKA |
Possible |
PlasmoGEM (Barseq) | PlasmoGEM | |
P. berghei ANKA |
Possible |
RMgm-4937 | Imported from RMgmDB | |
P. yoelii yoelii 17X |
Possible |
RMgm-1413 | Imported from RMgmDB |
Species | Stage | Phenotype | Reference | Submitter |
---|---|---|---|---|
P. berghei ANKA | Asexual |
No difference |
PlasmoGEM (Barseq) | PlasmoGEM |
P. berghei ANKA | Asexual |
No difference |
RMgm-4937 | Imported from RMgmDB |
P. berghei ANKA | Gametocyte |
No difference |
RMgm-4937 | Imported from RMgmDB |
P. berghei ANKA | Ookinete |
No difference |
RMgm-4937 | Imported from RMgmDB |
P. berghei ANKA | Oocyst |
No difference |
RMgm-4937 | Imported from RMgmDB |
P. berghei ANKA | Sporozoite |
No difference |
RMgm-4937 | Imported from RMgmDB |
P. berghei ANKA | Liver |
Difference from wild-type |
RMgm-4937
Normal infectivity of sporozoites to hepatocytes in vitro and in vivo. Mutant parasites develop into large, mature liver stages with extensive nuclear division and expression of merozoite specific proteins, such as msp1 and ama1. Most of the parasites arrest growth, however, just before the formation of infective merozoites. Only after intravenously infection of mice with high doses of sporozoites (2x10(5)) some of the mice (3 out of 10) developed blood infections with a greatly prolonged prepatent period (12-14 days). |
Imported from RMgmDB |
P. falciparum 3D7 | Asexual |
Attenuated |
32484795 (Conditional)
\". Robust exoerythrocytic schizogony with extensive cell growth and DNA replication was observed for P. falciparum mei2- liver stages in human liver-chimeric mice. However, P. falciparum mei2- liver stages failed to complete development and did not form infectious exoerythrocytic merozoites, thereby preventing their transition to asexual blood stage infection. Therefore, P. falciparum mei2- is a replication-competent, attenuated human malaria parasite strain with potentially increased potency, useful for vaccination to protect against P. falciparum malaria infection.\" |
Theo Sanderson, Francis Crick Institute |
P. yoelii yoelii 17X | Asexual |
No difference |
RMgm-1413 | Imported from RMgmDB |
P. yoelii yoelii 17X | Sporozoite |
No difference |
RMgm-1413 | Imported from RMgmDB |
P. falciparum 3D7 | Liver |
Possible |
32484795 (Conditional)
\". Robust exoerythrocytic schizogony with extensive cell growth and DNA replication was observed for P. falciparum mei2- liver stages in human liver-chimeric mice. However, P. falciparum mei2- liver stages failed to complete development and did not form infectious exoerythrocytic merozoites, thereby preventing their transition to asexual blood stage infection. Therefore, P. falciparum mei2- is a replication-competent, attenuated human malaria parasite strain with potentially increased potency, useful for vaccination to protect against P. falciparum malaria infection.\" |
Theo Sanderson, Francis Crick Institute |
P. yoelii yoelii 17X | Liver |
Difference from wild-type |
RMgm-1413
Plasmei2 sporozoites failed to initiate a blood stage infection (after injection of 5x10(4) purified sporozoites). Abnormal development of liver stages. Growth arrest of late liver stages. |
Imported from RMgmDB |
PlasmoDB | PBANKA_1122300 |
GeneDB | PBANKA_1122300 |
Malaria Metabolic Pathways | Localisation images Pathways mapped to |
Previous ID(s) | PB001281.02.0, PBANKA_112230 |
Orthologs | PCHAS_1121800 , PF3D7_0623400 , PKNH_1126800 , PVP01_1126100 , PVX_114285 , PY17X_1123700 |
Google Scholar | Search for all mentions of this gene |