Mutant/mutation
The mutant lacks expression of ICP (inhibitor of cysteine proteases). The mutant was cloned from mutant RMgm-1113 after excision of (part of) the icp locus by by using the Flp/FRT site-specific recombination (SSR) system.

Protein (function)
An endogenous cysteine protease inhibitor has been identified in P. falciparum, Pf-ICP (PF3D7_0911900; Falstatin). A recombinant  Pf-ICP expressed in E. coli was shown to potently inhibit a number of host proteases by in vitro protease activity assays. Additionally, Pf-ICP also inhibited several parasite proteases in these assays, including falcipain-2 and falcipain-3, but not falcipain-1. Search the database with the P. falciparum icp gene model  PF3D7_0911900 for additional mutants expressing tagged forms of ICP in rodent parasites or mutants lacking expression of ICP.

Phenotype
Asexual blood infections in mice induced infections with a delayed increase of the parasitemia.
Normal numbers of oocyst-derived (hemocoel) sporozoites are formed. Sporozoites have greatly impaired gliding motility and capacity to invade salivary glands. Sporozoites are not able to invade hepatocytes in vitro. Sporozoites were not infectious to mice.

See also RMgm-970 for an independent mutant lacking expression of ICP. This mutant showed a comparable phenotype of the lack of gliding motility and salivary gland invasion of sporozoites. No differences with wild type were detected in blood stage infections.

Analysis of 'conditional knock-out' mutant of ICP provided evidence for an additional role of ICP during liver stage development (see RMgm-1113)

Additional information
Evidence is presented that in mutant sporozoites CSP and TRAP are processed different from CSP and TRAP in wild type sporozoites, possibly by premature processing in the absence of the cysteine protease inhibitor ICP.

Other mutants
Click on PF3D7_0911900 for other mutants lacking icp or expressing tagged-forms of ICP