It is generally accepted that the mitochondria play central roles in energy 
production of most eukaryotes. In contrast, it has been thought that Plasmodium 
spp., the causative agent of malaria, rely mainly on cytosolic glycolysis but 
not mitochondrial oxidative phosphorylation for energy production during blood 
stages. However, Plasmodium spp. possesses all genes necessary for the 
tricarboxylic acid (TCA) cycle and most of the genes for electron transport 
chain (ETC) enzymes. Therefore, it remains elusive whether oxidative 
phosphorylation is essential for the parasite survival. To elucidate the role of 
TCA metabolism and ETC in malaria parasites, we deleted the gene for 
flavoprotein (Fp) subunit, Pbsdha, one of four components of complex II, a 
catalytic subunit for succinate dehydrogenase activity. The Pbsdha(-) parasite 
grew normally at blood stages in mouse. In contrast, ookinete formation of 
Pbsdha(-) parasites in the mosquito stage was severely impaired. Finally, 
Pbsdha(-) ookinetes failed in oocyst formation, leading to complete malaria 
transmission blockade. These results suggest that malaria parasite may switch 
the energy metabolism from glycolysis to oxidative phosphorylation to adapt to 
the insect vector where glucose is not readily available for ATP production.