Stage-specific depletion of myosin A supports an essential role in motility of malarial ookinetes.

摘要: Summary Functional analysis of Plasmodium genes by clas- sical reverse genetics is currently limited to mutants that are viable during erythrocytic schizogony, the pathogenic phase malaria parasite where transfection performed. Here, we describe a conceptually simple experimental approach study function essential asexual blood stages in subsequent life cycle stage promoter-swap approach. As proof concept targeted unconventional class XIV myosin MyoA, which known be required for Toxoplasma gondii tachyzoite loco- motion and host cell invasion. By placing cor- responding berghei gene, PbMyoA, under control apical membrane antigen 1 (AMA1) promoter, expression maintained but switched off transmission insect vector, i.e. ookinetes. In those mutant ookinetes gliding motility entirely abolished resulting complete block progres- sion Anopheles mosquitoes. Similar approaches should permit gene mosquito forms shared with erythro- cytic parasite.