PT  - JOURNAL ARTICLE
AU  - Souad Amiar
AU  - Nicholas J. Katris
AU  - Laurence Berry
AU  - Sheena Dass
AU  - Melanie J. Shears
AU  - Camille Brunet
AU  - Bastien Touquet
AU  - Mohamed-Ali Hakimi
AU  - Geoffrey I. McFadden
AU  - Yoshiki Yamaryo-Botté
AU  - Cyrille Y. Botté
TI  - Division and adaptation to host nutritional environment of apicomplexan parasites depend on apicoplast lipid metabolic plasticity and host organelles remodelling
AID  - 10.1101/585737
DP  - 2019 Jan 01
TA  - bioRxiv
PG  - 585737
4099  - http://biorxiv.org/content/early/2019/03/22/585737.short
4100  - http://biorxiv.org/content/early/2019/03/22/585737.full
AB  - Apicomplexan parasites are unicellular eukaryotes responsible for major human diseases including malaria and toxoplasmosis. Apicomplexan parasites must obtain and combine lipids both from host cell scavenging and de novo synthesis to maintain parasite propagation and survival within their human host. Major questions on the actual role for each lipid source or how these are regulated upon fluctuating host nutritional conditions remain unanswered. Characterization of an apicoplast acyltransferase TgATS2, shows that the apicoplast provides local (lyso)phosphatidic acid balance, which is required for the recruitment of a novel dynamin (TgDrpC) critical during parasite cytokinesis. Disruption of TgATS2 led parasites to shift metabolic lipid acquisition from de novo synthesis towards host scavenging. Importantly, both lipid scavenging and de novo synthesis pathways exhibit major metabolic and cellular plasticity upon sensing host lipid-deprived environments through concomitant (i) up-regulation of de novo fatty acid synthesis capacities in the apicoplast, and (ii) parasite-driven host cell remodelling to generate multi-membrane-bound structures from host organelles that are imported towards the parasite.