Not Open Access | PI(3)P-independent and -dependent pathways function together in a vacuolar translocation sequence to target malarial proteins to the host erythrocyte
We have previously shown that the R to A mutation in the HT motif, abrogates VTS binding to PI(3)P (Kd > 5 μM). We now show that remarkably, the R to A mutant is exported to the host erythrocyte, for both membrane and soluble reporters, although the efficiency of export is reduced to ∼30% of that seen with a complete VTS.