Search bioRxiv⌕ Search

Biology subjects

Holland, L. K. K.

Publications and source records attributed to Holland, L. K. K..

2 recordsLinked to original sources

Lipid Landscape of human cells

Eukaryotic cells synthesise thousands of lipid species, yet the principles that organise them across compartments remain unclear. Here we introduce PAP-SL, parallel (immuno)affinity purification coupled to shotgun lipidomics, to map [~]300 lipid species across six compartments of human cells and uncover general rules of lipid organisation. Correlation analyses of stoichiometric lipid compositions resolved archetypal distribution trajectories. Biosynthetic origin set the baseline: mitochondrial and lysosomal pathways generated confined pools, whereas the ER acted as a dispatch hub shaping downstream membrane territories. The ER established the saturated plasma membrane through transfer of phosphatidylserine, sphingolipids, and cholesterol, together with species-level selection of more saturated glycerophospholipids across diverse headgroups, while less-saturated species moved unselectively into mitochondria. The ER also channelled ether-linked glycerophospholipids to lysosomes, forming a territory dominated by ether phosphatidylcholine that collapsed under ethanolamine-driven metabolic rewiring. PAP-SL defines a framework to resolve lipid organisation and its metabolic plasticity in health and disease.

systems biology↗

Lysosome repair by ER-mediated cholesterol transfer

Lysosome integrity is essential for cell viability, and lesions in lysosome membranes are repaired by the ESCRT machinery. Here we describe an additional mechanism for lysosome repair that is activated independently of ESCRT recruitment. Lipidomic analyses showed increases in lysosomal phosphatidylserine and cholesterol after damage. Electron microscopy demonstrated that lysosomal membrane damage is rapidly followed by formation of contacts with the endoplasmic reticulum (ER), which depend on the ER proteins VAPA/B. The cholesterol-binding protein ORP1L was recruited to damaged lysosomes, accompanied by cholesterol accumulation by a mechanism that required VAP-ORP1L interactions. The PtdIns 4-kinase PI4K2A rapidly produced PtdIns4P on lysosomes upon damage, and knockout of PI4K2A inhibited damage-induced accumulation of ORP1L and cholesterol and led to failure of lysosomal membrane repair. The cholesterol-PtdIns4P transporter OSBP was also recruited upon damage, and its depletion caused lysosomal accumulation of PtdIns4P and resulted in cell death. We conclude that ER contacts are activated on damaged lysosomes in parallel to ESCRTs to provide lipids for membrane repair, and that PtdIns4P generation and removal are central in this response.

cell biology↗