Mutant/mutation
The mutant lacks expression of the P52 (P36p) and P36 protein and expresses the reporter protein GFP. Both genes have been disrupted  using a single DNA construct (double knock-out mutant). The genes have been disrupted in a reporter mutant (676m1cl1; RMgm-29) that expresses GFP constitutively throughout the life cycle

Protein (function)
P52 (P36p) and P36 are members of a small family of proteins, the 6-cysteine (cys) family of (surface) proteins (Thompson J. et al., Mol. Biochem. Parasitol. (2001)118, 147-54). The proteins are characterised by domains of roughly 120 amino acids in size that contain six positionally conserved cysteines (6-cys). Although some species of Plasmodium (may) contain unique members of the 6-cys family, ten members have been identified that are conserved both in structure as well as in genome organisation throughout the genus. Some of the conserved 6-cys proteins are encoded by genes that form paralogous gene-pairs which are closely linked in the genome separated by less then 2 kb of intergenic region. Most members have a GPI anchor and are predicted membrane surface proteins whereas others appear to be secreted and most members are expressed in a discrete stage-specific manner in gametocytes, sporozoites or merozoites.

Phenotype
P36 and p52  (p36p) are paralogous genes, located in tandem next to each other. Both genes have been disrupted  using a single DNA construct (double knock-out mutant).
Gliding motility, hepatocyte traversal and hepatocyte invasion in vitro (HepG2) of mutant sporozoites is similar to wild type sporozoites. Liver stage development is strongly impaired and parasites do not develop into the schizont stage and most invaded parasites cannot be detected anymore at 24 hours after infection. Inside the hepatocytes the formation of a parasitophourous vacuole is not detected at 15 and 24h after infections as shown by staining with antibodies against the parasithophorous vacuole membrane proteins.
The early arrest of Δp52+p36 parasites after hepatocyte invasion is similar to the phenotype reported for P. berghei mutants lacking expression of only P52 and P. yoelii mutants lacking both P52 and P36 (see below).
Infection of mice (C57BL/6) by bite of infected mosquitoes did not result in blood stage infection. Infection of BALB/c mice by intravenous injection of 50.000 sporozoites did not result in blood stage infection. Only intravenous inoculation of 50.000 sporozoites in C57BL/6 mice resulted in blood stage infection in a low percentage (10-20%) of mice.

Additional information

Other mutants
An independent P. berghei mutant lacking the expression of both P52 (P36p) and P36 (RMgm-42)
P. berghei mutants lacking expression of P52 (P36p) (RMgm-40, RMgm-41, RMgm-44).
P. berghei mutants lacking expression of P36 (RMgm-45; RMgm-353).
A P. yoelii mutant (RMgm-43) lacking the expression of both P52 (P36p) and P36.