Résumé
During the erythrocytic cycle of the malaria parasite Plasmodium falciparum, egress and invasion are essential steps finely controlled by reversible phosphorylation. In contrast to the growing number of kinases identified as key regulators, phosphatases have been poorly studied, and calcineurin is the only one identified so far to play a role in invasion. PfShelph2, a bacterial-like phosphatase, is a promising candidate to participate in the invasion process, as it was reported to be expressed late during the asexual blood stage and to reside within an apical compartment, yet distinct from rhoptry bulb, micronemes, or dense granules. It was also proposed to play a role in the control of the red blood cell membrane deformability at the end of the invasion process. However, genetic studies are still lacking to support this hypothesis. Here, we take advantage of the CRISPR-Cas9 technology to tag shelph2 genomic locus while retaining its endogenous regulatory regions. This new strain allows us to follow the endogenous PfShelph2 protein expression and location during asexual blood stages. We show that PfShelph2 apical location is also distinct from the rhoptry neck or exonemes. We further demonstrate PfShelph2 dispensability during the asexual blood stage by generating PfShelph2-KO parasites using CRISPR-Cas9 machinery. Analyses of the mutant during the course of the erythrocytic development indicate that there are no detectable phenotypic consequences of Pfshelph2 genomic deletion. As this lack of phenotype might be due to functional redundancy, we also explore the likelihood of PfShelph1 (PfShelph2 paralog) being a compensatory phosphatase. We conclude that despite its cyclic expression profile, PfShelph2 is a dispensable phosphatase during the Plasmodium falciparum asexual blood stage, whose function is unlikely substituted by PfShelph1.