Mutant/mutation
The mutant lacks expression of the P52 (P36p) and P36 protein.

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). The phenotype analysis demonstrates a role of these proteins in liver stage development. Gliding motility, hepatocyte Invasion and traversal hepatocyte of mutant sporozoites is similar to wild type sporozoites. Inside the host hepatocyte development is arrested very soon after invasion.

Additional information
P. yoelii 'attenuated sporozoites' lacking expression of P36/P52 can induce sterile (protective) immunity in mice against challenge with wild type sporozoites by immunization of mice (BALB/c, C57Bl/6) with the mutant sporozoites.
Infection of mice by intravenously injection of high numbers of 'single knock-out' P. berghei mutants lacking either P52 (P36p) or P36 can result in a blood stage infection in a small number of mice ('breakthrough parasites'). No such breakthrough parasites were observed in the double knock-out P. yoelii mutant lacking expression of both proteins.

Other mutants
P. berghei mutants have been generated that lack expression of P52 (P36p) (RMgm-40, RMgm-41, RMgm-44).
P. berghei mutants have been generated that lack expression of P36 (RMgm-45; RMgm-353). A P. berghei mutant (RMgm-42) has been generated that lacks the expression of both P36p (P52) and P36.
In P. falciparum a mutant has been generated lacking P52 (PFD0215c; van Schaijk et al., (2008) PloS ONE 3(10):e3549). The 'arrested' phenotype of liver stage of this P. falciparum mutant in primary human hepotocytes is similar to the phenotype of P. berghei and P. yoelii mutants lacking expression of P52 (P36p).