Open AccessType II fatty acid synthesis is essential only for malaria parasite late liver stage development
Author(s) -
Vaughan Ashley M.,
O'Neill Matthew T.,
Tarun Alice S.,
Camargo Nelly,
Phuong Thuan M.,
Aly Ahmed S. I.,
Cowman Alan F.,
Kappe Stefan H. I.
Publication year - 2009
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.1462-5822.2008.01270.x
Subject(s) - biology , apicoplast , plasmodium yoelii , malaria , parasite hosting , plasmodium (life cycle) , plasmodium falciparum , intracellular parasite , fatty acid synthesis , fatty liver , virology , enzyme , intracellular , microbiology and biotechnology , immunology , biochemistry , apicomplexa , disease , parasitemia , medicine , world wide web , computer science
Summary Intracellular malaria parasites require lipids for growth and replication. They possess a prokaryotic type II fatty acid synthesis (FAS II) pathway that localizes to the apicoplast plastid organelle and is assumed to be necessary for pathogenic blood stage replication. However, the importance of FAS II throughout the complex parasite life cycle remains unknown. We show in a rodent malaria model that FAS II enzymes localize to the sporozoite and liver stage apicoplast. Targeted deletion of FabB/F , a critical enzyme in fatty acid synthesis, did not affect parasite blood stage replication, mosquito stage development and initial infection in the liver. This was confirmed by knockout of FabZ , another critical FAS II enzyme. However, FAS II‐deficient Plasmodium yoelii liver stages failed to form exo‐erythrocytic merozoites, the invasive stage that first initiates blood stage infection. Furthermore, deletion of FabI in the human malaria parasite Plasmodium falciparum did not show a reduction in asexual blood stage replication in vitro . Malaria parasites therefore depend on the intrinsic FAS II pathway only at one specific life cycle transition point, from liver to blood.