Mutant/mutation
The mutant lacks expression of CDPK3 (calcium-dependent protein kinase 3).

Protein (function)
CDPK3 belongs to an expanded family of Ca²⁺ dependent protein kinases (CDPKs). CDPKs combine an amino-terminal serine/threonine kinase domain and a carboxy-terminal calmodulin-like domain, composed of four EF hands, in the same molecule. In plants, CDPKs translate Ca²⁺ signals generated by external stimuli into cellular responses, thereby regulating cell division and differentiation, the development of tolerance to stress stimuli and the specific defense responses to pathogens.

Phenotype
The phenotype analyses indicate a role of CDPK3 in the transformation of the mature ookinete into the oocyst stage. Specifically, ookinetes fail to bind and traverse the cell of the midgut wall and the motility of ookinetes is strongly affected.
Motility of  ookinetes was abnormal, showing frequent flexing, bending, twirling and pendular motions, but only rare bouts of translocation over short distances.
Injection of in vitro cultured, mature ookinetes into the hemocoel and thereby by-passing the midgut wall resulted in normal development of oocysts and infectious sporozoites, indicating that the role of CDPK3 is restricted to the ookinete stage.
These analyses suggest a role for CDPK3 in regulating productive gliding motility of ookinetes.

Additional information
An independent mutant lacking expression of CDPK3, RMgm-165, has been generated which show a comparable defect in ookinete to oocyst transition. However, instead of a general defect in  motility of the ookinetes it has been suggested on basis of the phenotype analysis that ookinetes are affected in a CDPK3-dependent mode of motility that is required to penetrate the layer surrounding the blood meal.
The cdpk3- parasite has been complemented by introducing an episomal plasmid in which the complete cdpk3 genomic sequence was fused to a double c-myc epitope tag (c-terminal tag) The plasmid was introduced by electroporation and maintained as an episome by selection for the hdhfr gene with WR99210. Complementation fully restored the infectivity of ookinetes.

Disruption of the P. falciparum ortholog has been attempted (Solyakov et al., 2011, Nat Commun, 2:565).
The gene is likely essential for asexual proliferation. After transfection with a KO vector a weak PCR signal diagnostic for integration was observed, indicating that integration does transiently occur but parasites with a disrupted locus do not persist. Cloning will be required to validate this interpretation for this gene.

Other mutants
RMgm-165: An independent mutant lacking expression of CDPK3
RMgm-168: A mutant lacking expression of CDPK3 and expressing GFP under control of the hsp70 promoter. This mutant has been generated by crossing mutant RMgm-165 lacking expression of CDPK3 with mutant RMgm-166 that expresses GFP.
RMgm-12: A mutant lacking expression CDPK4