Mutant/mutation
The mutant lacks expression of the P36p protein.

Protein (function)
P36p is a member 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.
A paralogue of the p36p gene, p36 (PB000892.00.0; pbs36), is located in the genome next to p36p (in tandem).

Phenotype
The phenotype analysis demonstates a role of this protein 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. berghei 'attenuated sporozoites' lacking expression of P36p 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.

Host hepatocyte apoptosis is normally inhibited by wild type sporozoites upon invasion and establishment of the parasitophorous vacuole. The rapid disappearance of cells infected with the mutant sporozoites might be due to the inability of the mutant to prevent apoptosis of the host cell. The level of apoptosis in hepatocytes infected with mutant sporozoites was significantly higher than in hepatocytes infected with wild type sporozoites.

Disruption of the P. falciparum ortholog of P36p, P52 (PFD0215c) results in a comparable phenotype of the sporozoites that become similarly arrested during liver stage development (van Schaijk, B.C. et al., 2008, PloS ONE, 3:e3549)

 Other mutants
A P. berghei mutant has been generated that lacks expression of this protein and in addition expresses the reporter protein GFP constitutively throughout development (RMgm-41).
An independent P. berghei mutant has been generated that lacks expression of this protein (RMgm-44).
A P. berghei mutant (RMgm-42) has been generated that lacks the expression of not only this protein but also its paralogue P36 (PB000892.00.0; pbs36).
A P. yoelii mutant (RMgm-43) has been generated that lacks the expression of not only this protein but also its paralogue P36 (PY01341; p36).
In P. falciparum a mutant has been generated lacking this protein (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 the P. berghei mutant.