Mutant/mutation
The mutant lacks expression of FABI. The mutant has been generated using the same DNA construct to generate the published mutant RMgm-197.

Protein (function)
FABI is an enzyme of the bacterial like type II fatty acid biosynthesis (FAS-II) pathway. In Plasmodium FAS-II enzymes have been localized to the apicoplast, a nonphotosynthetic plastid organelle of cyanobacterial origin.
FAS-II requires acetyl-Coenzyme A (CoA), which can be converted from pyruvate by the pyruvate dehydrogenase complex. Acetyl-CoA carboxylase converts acetyl-CoA to malonyl-CoA, which is tethered to an acyl carrier protein (ACP) by malonyl-CoA:ACP transacylase (FabD). This produces malonyl-ACP, which, in conjunction with acetyl-CoA, is acted upon by β-ketoacyl-ACP synthase III (Fab H) to form β-ketoacyl-ACP. This precursor enters the FAS-II elongation cycle, mediated by FabB/F (β-ketoacyl-acyl-carrier-protein (ACP) synthase), FabG (β-ketoacyl-ACP reductase), FabZ/A (β-hydroxyacyl-ACP dehydratase), and FabI (trans-2-enoyl-ACP reductase). These four FAS-II enzymes iteratively catalyze the addition of two carbon chains to a growing fatty acyl carbon chain via condensation, reduction, dehydration, and reduction steps, respectively.

The phenotype analyses of another mutant lacking FABI.(RMgm-197) show that FABI is not essential for blood stage development, mosquito stage development and initial infection of the liver. The results indicate a key role of FABI in the formation of infective liver stage merozoites demonstrating the importance of FASII pathway for synthesis of fatty acids during late liver stage development.

Phenotype
The phenotype has not been analysed in detail. The mutant has been generated using the same DNA construct to generate the published mutant RMgm-197. See RMgm-197 for a detailed description of the phenotype of a mutant lacking FABI.

Additional information

Other mutants
RMgm-197: A mutant lacking expression of FABI
RMgm-180: A mutant expressing myc tagged FABI