Background: Glycerophosphocholine (GroPCho) is a phospholipid metabolite found throughout the human body. Results: Loss of Git3 and Git4 in C. albicans abolishes GroPCho transport, and Git3-deficient cells exhibit reduced virulence. Conclusion: The major GroPCho transporter, Git3, is required for full virulence. Significance: This report is the first to identify a eukaryotic GroPCho-specific transporter and the first to implicate GroPCho utilization in pathogenicity.

Background: Ypk1 is a protein kinase known to regulate sphingolipid homeostasis. Plb1 deacylates phosphatidylcholine to produce glycerophosphocholine. Results: Loss of Ypk1 or disruption of sphingolipid synthesis by other means elevates Plb1-mediated phosphatidylcholine turnover. Conclusion: Accelerated turnover of phosphatidylcholine compensates for aberrant sphingolipid synthesis. Significance: Sphingolipid synthesis is coordinated with phosphatidylcholine metabolism to maintain membrane lipid homeostasis.