The flexibility of Apicomplexa parasites in lipid metabolism

Abstract

Apicomplexa are obligate intracellular parasites responsible for major human infectious diseases such as toxoplasmosis and malaria, which pose social and economic burdens around the world. To survive and propagate, these parasites need to acquire a significant number of essential biomolecules from their hosts. Among these biomolecules, lipids are a key metabolite required for parasite membrane biogenesis, signaling events, and energy storage. Parasites can either scavenge lipids from their host or synthesize them de novo in a relict plastid, the apicoplast. During their complex life cycle (sexual/asexual/dormant), Apicomplexa infect a large variety of cells and their metabolic flexibility allows them to adapt to different host environments such as low/high fat content or low/high sugar levels. In this review, we discuss the role of lipids in Apicomplexa parasites and summarize recent findings on the metabolic mechanisms in host nutrient adaptation.

Disrupting the plastidic iron-sulfur cluster biogenesis pathway in Toxoplasma gondii has pleiotropic effects irreversibly impacting parasite viability

“…There is now published evidence that parasites can adapt their metabolic capacities depending on the nutrient environment (46,47,64), and even survive in vitro when FASII enzymes are inactivated (48,65). There is clearly flexibility in the adaptation of parasite pathways to lipid J o u r n a l P r e -p r o o f sources (46,47,66). As tachyzoites can readily scavenge and incorporate FAs from exogenous sources (i.e.…”

“…There is now published evidence that parasites can adapt their metabolic capacities depending on the nutrient environment ( 46 , 47 , 64 ) and even survive in vitro when FASII enzymes are inactivated ( 48 , 65 ). There is clearly flexibility in the adaptation of parasite pathways to lipid sources ( 46 , 47 , 66 ). As tachyzoites can readily scavenge and incorporate FAs from exogenous sources (i.e., phospholipid made by the host cell and/or phospholipids and FA scavenged from the extracellular medium) into their own range of lipids ( 46 , 47 , 48 , 67 ), in the end the essentiality of the FASII pathway depends largely on nutrient availability in vivo or in vitro through culture conditions provided ( 64 ).…”

Disrupting the plastid-hosted iron-sulfur cluster biogenesis pathway in Toxoplasma gondii has pleiotropic effects irreversibly impacting parasite viability

“…While it is undoubtedly a metabolic pathway that plays a central role for parasite fitness, the view on the essentiality of FASII in T. gondii tachyzoites has recently evolved. There is now published evidence that parasites can survive in vitro even when FASII enzymes are inactivated (44, 59) and there is clearly flexibility in the adaptation to lipid sources (60). As tachyzoites can readily scavenge and incorporate FAs from exogenous sources into their own range of lipids (43, 44, 61), in the end the essentiality of the FASII pathway depends largely on the culture conditions.…”

“…There is now published evidence that parasites can adapt their metabolic capacities depending on the nutrient environment (44, 45), and even survive in vitro when FASII enzymes are inactivated (46, 60). There is clearly flexibility in the adaptation of parasite pathways to lipid sources (44, 45, 61). As tachyzoites can readily scavenge and incorporate FAs from exogenous sources (i.e.…”

Role of Host Small GTPases in Apicomplexan Parasite Infection

“…Apicomplexa also scavenge sphingolipids, fatty acids and phospholipids from the host and produce their own lipids through a relic plastid called apicoplast. Upon acquisition from the host, the acquired lipids are often assembled together with parasite lipids in order to generate most lipid species important for parasite needs [ 8 ].…”