Open AccessStage‐specific depletion of myosin A supports an essential role in motility of malarial ookinetes
Author(s) -
SidenKiamos Inga,
Ganter Markus,
Kunze Andreas,
Hliscs Marion,
Steinbüchel Marion,
Mendoza Jacqueline,
Sinden Robert E.,
Louis Christos,
Matuschewski Kai
Publication year - 2011
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2011.01686.x
Subject(s) - biology , plasmodium berghei , schizogony , plasmodium (life cycle) , microbiology and biotechnology , gene , gliding motility , transfection , microneme , mutant , motility , malaria , virology , plasmodium falciparum , apicomplexa , genetics , parasite hosting , immunology , world wide web , computer science
Summary Functional analysis of Plasmodium genes by classical reverse genetics is currently limited to mutants that are viable during erythrocytic schizogony, the pathogenic phase of the malaria parasite where transfection is performed. Here, we describe a conceptually simple experimental approach to study the function of genes essential to the asexual blood stages in a subsequent life cycle stage by a promoter‐swap approach. As a proof of concept we targeted the unconventional class XIV myosin MyoA , which is known to be required for Toxoplasma gondii tachyzoite locomotion and host cell invasion. By placing the corresponding Plasmodium berghei gene, PbMyoA , under the control of the apical membrane antigen 1 ( AMA1 ) promoter, expression in blood stages is maintained but switched off during transmission to the insect vector, i.e. ookinetes. In those mutant ookinetes gliding motility is entirely abolished resulting in a complete block of life cycle progression in Anopheles mosquitoes. Similar approaches should permit the analysis of gene function in the mosquito forms that are shared with the erythrocytic stages of the malaria parasite.