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Moodie, L. W. K.

Publications and source records attributed to Moodie, L. W. K..

2 recordsLinked to original sources

Membrane contacts between caveolae and the endoplasmic reticulum regulate uptake and metabolic trapping of long-chain fatty acids

The vital process of cellular fatty acid metabolism involves uptake, metabolic trapping and storage of long-chain fatty acids (LCFAs) in different lipid species. Although several different enzymes like transporters and acyl-CoA synthetases are involved, the sequential mechanistic steps of the process are poorly understood. Here, we have addressed the role of the caveola coat protein caveolin1 and the acyl-CoA synthetase FATP1 in the process as both have major impacts in the uptake and storage of fatty acids in vivo and in vitro. Using live cell microscopy and mass spectrometry-based quantification of LCFA metabolism, we found that FATP1-mediated uptake and metabolic processing of LCFAs is coupled to, and dependent on caveolin1. Furthermore, both proteins stimulate the incorporation of LCFA into phospholipids and triacylglycerol, but not in sphingolipids. Using correlative light and electron microscopy we found that membrane contact sites are formed between FATP1-enriched endoplasmic reticulum (ER) and caveolae. Analysis of their temporal stability showed that they are dynamic but frequently persist over minutes. We propose that caveolae directly couple the plasma membrane (PM) to the ER for directed LCFA transport and metabolic processing.

cell biology↗

Lipid accumulation promotes scission of caveolae

Caveolae, bulb-shaped invaginations of the plasma membrane (PM), show distinct behaviors of scission and fusion at the cell surface. Although it is known that caveolae are enriched in cholesterol and sphingolipids, exactly how lipid composition influences caveolae surface stability has not yet been elucidated. Accordingly, we inserted specific lipids into the PM of cells via membrane fusion and studied acute effects on caveolae dynamics. We demonstrate that cholesterol and glycosphingolipids specifically accumulate in caveolae, which decreases their neck diameter and drives their scission from the cell surface. The lipid-induced scission was counteracted by the ATPase EHD2. We propose that lipid accumulation in caveolae generates an intrinsically unstable domain prone to scission if not balanced by the restraining force of EHD2 at the neck. Our work advances the understanding of how lipids contribute to caveolae dynamics, providing a mechanistic link between caveolae and their ability to sense the PM lipid composition. SUMMARYCaveolae serve as mechanoprotectors and membrane buffers but their specific role in sensing plasma membrane lipid composition remains unclear. Hubert et al. show that cholesterol and glycosphingolipids accumulate in caveolae and drive subsequent scission from the cell surface. These results provide new insight into how lipids contribute to budding and scission of membrane domains in cells.

biochemistry↗