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Courtney, K.

Publications and source records attributed to Courtney, K..

2 recordsLinked to original sources

Fluorescence imaging-induced phospholipid oxidation drives membrane phase separation by shifting miscibility boundaries

Fluorescence microscopy is a widely used tool for visualizing membrane organization in model and cellular systems; however, photoexcitation during imaging can generate reactive oxygen species, thereby altering membrane structure. Here, we show that fluorescence imaging actively drives membrane phase separation through photo-induced phospholipid oxidation. Using giant unilamellar vesicles, we observed that illumination of initially homogeneous membranes triggers the emergence of coexisting liquid-ordered and liquid-disordered domains. Chemical analysis by thin layer chromatography and mass spectrometry revealed the formation of a complex mixture of oxidized lipid species following excitation, characterized by stepwise oxygen additions to unsaturated phospholipids and multiple degradation products. These modifications increase lipid polarity and disrupt acyl chain packing, reducing favorable interactions with saturated phospholipids. As a result, membranes near the miscibility boundary become prone to demixing upon illumination, indicating that photo-induced lipid oxidation effectively shifts the miscibility boundary. Consistent with this model, light-induced phase separation is highly sensitive to membrane composition, with maximal effects observed near the liquid-liquid miscibility boundary. Electroformation substrate further modulated this effect, suggesting that pre-existing oxidative conditions sensitize membranes to subsequent photo-induced changes. Together, these findings demonstrate that excitation light can introduce artifacts in membrane phase behaviour. More broadly, subtle chemical modifications of phospholipids can shift membrane miscibility and reorganize membrane structure.

biochemistry↗

Cellular genome wide association study identifies common genetic variation influencing lithium induced neural progenitor proliferation

Lithium is used in the treatment of bipolar disorder (BD) and is known to increase neural progenitor cell (NPC) proliferation. Though the mechanism of lithiums therapeutic effect is not understood, evidence suggests that genetic variation influences response to treatment. Here, we used a library of genetically diverse human NPCs to identify common genetic variants that modulate lithium induced proliferation. We identified a locus on chr3p21.1 associated with lithium induced proliferation that colocalizes with BD risk. One lithium responsive gene, GNL3, was detected within the locus. The allele associated with increased baseline and lithium-induced GNL3 expression was also associated with increased lithium-induced NPC proliferation. Experimental manipulation of GNL3 expression using CRISPRa/i in NPCs showed that GNL3 was necessary for lithiums full proliferative effects, and sufficient to induce proliferation without lithium treatment. In all, our data suggest that GNL3 expression sensitizes NPCs for a stronger proliferative response to lithium.

genetics↗