Abstract
The malaria parasite, Plasmodium falciparum, harbours a relict plastid known as the ‘apicoplast’. The discovery of the apicoplast ushered in an exciting new prospect for drug development against the parasite. The eubacterial ancestry of the organelle offers a wealth of opportunities for the development of therapeutic interventions. Morphological, biochemical and bioinformatic studies of the apicoplast have further reinforced its ‘plant-like’ characteristics and potential as a drug target. However, we are still not sure why the apicoplast is essential for the parasite's survival. This review explores the origins and metabolic functions of the apicoplast. In an attempt to decipher the role of the organelle within the parasite we also take a closer look at the transporters decorating the plastid to better understand the metabolic exchanges between the apicoplast and the rest of the parasite cell.
Highlights
The apicoplast is a vestigial plastid present in most parasites of the Phylum Apicomplexa
In contrast to FASII, the DOXP pathway for isoprenoid biosynthesis in the apicoplast appears to be essential to blood-stage parasites as the antibiotic fosmidomycin, an inhibitor of IspC (Kuzuyama et al 1998), is effective in managing the clinical symptoms of malaria that are associated with the intra-erythrocytic phase of parasites (Jomaa et al 1999)
Considering the lack of other candidates in the inner pair of apicoplast membranes, these two transporters PfoTPT and PfiTPT are postulated to work in tandem to facilitate the import of triose phosphates and PEP to channel the substrates into the FASII and isoprenoid biosynthesis pathways but how such substrates cross the middle two apicoplast membranes remains unclear (Mullin et al 2006; Lim et al 2009)
Summary
The apicoplast is a vestigial plastid present in most parasites of the Phylum Apicomplexa. In contrast to FASII, the DOXP pathway for isoprenoid biosynthesis in the apicoplast appears to be essential to blood-stage parasites as the antibiotic fosmidomycin, an inhibitor of IspC (Kuzuyama et al 1998), is effective in managing the clinical symptoms of malaria that are associated with the intra-erythrocytic phase of parasites (Jomaa et al 1999). It is, noteworthy that fosmidomycin is poorly effective against the coccidians E. tenella and T. gondii despite the presence of the isoprenoid genes in these parasites (Clastre et al 2007). It would appear strange for the parasite to back up its system as proposed but remains a possibility
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