Mutant/mutation
The mutant lacks expression of pbOGG1

Protein (function)
Base excision repair (BER) DNA N-glycosylase Plasmodium homologs EndoIII and Ogg1would putatively recognize DNA lesions prior to the action of apurinic/apyrimidinic (AP)-endonucleases. Both Ape1 and Apn1 endonucleases have earlier been shown to function solely in the parasite mitochondrion.

Phenotype
Normal growth/multiplication of blood stage parasite. Normal oocyst and sporozoite production.
Reduced infectivity of PbOgg1 KO sporozoites in C57BL/6 mice. The patency (time between inoculation of sporozoites and appearance of parasites in blood) was prolonged (1.5 to 2 day delay) in PbOgg1 KO sporozoite-injected mice. PbOgg1 KO EEFs develop and mature into hepatic merozoites normally. Mice inoculated with PbOgg1 KO merosomes showed a substantial delay in patency (time for appearance of parasite blood stages) of approximately 2 days. This indicates that PbOgg1 KO merosomes are released efficiently from infected hepatocytes, but they are less infective to red blood cells.

Additional information
To attempt localisation of Ogg1 in P. berghei, a transgenic parasite line (PbOgg1-3XHA) was generated by tagging PbOgg1 with a C-terminal 3XHA (hemagglutinin) tag. The prepared tagging construct was transfected in cultured P. berghei schizonts. After successful transfection, integration of the tagging cassette was confirmed using a site-specific integration PCR. However, western blotting of the parasite lysate with antiHA Ab detected a protein band of the expected size only upon very high exposure, indicating that expression levels of the HA-tagged PbOgg1 were very low and could not be reliably used for localisation by IFA.

Other mutants