The parasite Plasmodium falciparum causes the most severe form of malaria in humans. After invasion into erythrocytes, asexual
parasite stages drastically alter their host cell and export remodelling and virulence proteins. Previously, we have reported identification and functional analysis of a short motif necessary for export of proteins out
of the parasite and into the red blood cell. In this talk I will describe a generalised hidden Markov model algorithm, validated by expression of candidate proteins as GFP fusions, to define the "exportome" across the genus Plasmodium. Using it we have identified exported proteins conserved between malaria parasites of rodents and the two malaria lineages that infect primates represented by P.vivax and P.falciparum.. We have identified a novel gene family that shares a unique C-terminal
domain with >50 paralogs in P.falciparum and > 30 in P.vivax; however,there is only one member in each of the three rodent malaria species
studied. These data suggest radiation of genes encoding remodelling and virulence factors from a small number of loci in a common Plasmodium
ancestor, and imply a closer phylogenetic relationship between the two primate malaria lineages than previously believed. This talk reports the work of my student Toby Sargeant at the Walter & Eliza Hall Institute of Medical Research, and a number of biologists there.
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