Characterization of PF13_0027, a putative phosphatase in the human malaria parasite Plasmodium falciparum

Malaria is a continuing problem in both tropical and subtropical regions around the world affecting millions of people. This disease is caused by parasites of the genus Plasmodium, and has been a topic of numerous studies. Genomic analysis of Plasmodium has revealed vital information about the parasite biology and pathogenesis, however much of the encoded proteins remain uncharacterized. PF13_0027 is a conserved protein phosphatase expressed in all stages of development. A null PF13_0027 parasite revealed an altered cell cycle resulting in an attenuated growth phenotype. Genetic complementation rescued the wild-type phenotype and revealed that PF13_0027 is important for asexual development. Further analysis has uncovered that it may not participate in signal transduction but in a role characteristic of a pseudophosphatase. The conserved substitution of one of the catalytic residues suggests that it may retain substrate-trapping ability without dephosphorylation. Currently there is an urgent need for new antimalarials because of increasing resistance to common drugs and the absence of an effective vaccine. Blocking the expression of PF13_0027 to create a null parasite reduces the malaria parasite's ability to survive thus providing a novel drug target or an attenuated blood stage parasite vaccine. My role in this project: I am a doctoral candidate working on this project for my dissertation. I carried out the bioinformatics analysis, recombinant protein expression, literature review, phosphatase assays, and mutagenesis.