MFSD2A is an integral membrane protein highly expressed in the endothelial cells of the blood-brain barrier (BBB), where it transports essential ω-3 fatty acids, such as docosahexaenoic acid (DHA), into the brain in the form of lysophosphatidylcholine (LPC-DHA)1. In humans, mutations in MFSD2A are associated with severe neurological disorders, including microcephaly, intracranial hemorrhage and cognitive deficits2-4. Interestingly, recent studies indicate that MFSD2A has a broader physiological significance that extends beyond its ω-3 fatty acid transporter role. This project is focused on uncovering these diverse roles of MFSD2A by biochemically and structurally investigating its interactions with various putative ligands.
Aim 1 will investigate how lithium inhibits MFSD2A-mediated LPC-DHA transport1,5. Given that lithium is widely used as a treatment for bipolar disorder6, elucidating its effects on transporters such as MFSD2A could reveal new insights into how lithium influences brain lipid homeostasis. We have expressed and purified MFSD2A in lithium-containing buffer, confirmed Fab complex formation, and obtained initial cryo-EM 2D class averages of the Fab-bound transporter.
Aim 2 will focus on elucidating the molecular mechanism underlying MFSD2A-mediated transport of the antibiotic tunicamycin, which has been suggested to be an MFSD2A substrate7. Thus far, we have demonstrated in-house that tunicamycin binds to MFSD2A. Elucidation of this transport mechanism will help us understand the substrate promiscuity of MFSD2A and may pave the way for the design of molecules that can hijack the transporter to cross the BBB.
Aim 3 will structurally characterise the interaction between MFSD2A and the Zika virus envelope (ZIKV E) protein, which exploits MFSD2A as a receptor at the blood-brain barrier8. This aim will reveal how viral binding alters MFSD2A function and contributes to BBB disruption during Zika virus infection.