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DFCP1 Forms a Membrane Barrier That Organises Lysosome Repair Sites
A bioRxiv preprint reports that DFCP1 assembles into a helical coat that concentrates the membrane lipid PI3P and helps organise sites where cells repair damaged lysosomes.
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Recent reporting, analysis and explainers from the Cell Biology desk.
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A bioRxiv preprint reports that DFCP1 assembles into a helical coat that concentrates the membrane lipid PI3P and helps organise sites where cells repair damaged lysosomes.
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A bioRxiv preprint reports that Cell Painting PLUS uses additional organelle-resolved imaging to improve morphological profiling of compounds. In tests of 284 compounds in U2OS cells, it performed better than conventional Cell Painting for identifying compounds that interfere with lysosome function.
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A bioRxiv preprint reports that Plasmodium male-gamete axonemes retain key surface motility modules but have a reduced set of proteins inside their microtubule doublets. It also describes proteins involved in doublet organization and the progressive assembly of outer dynein arms.
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A bioRxiv preprint reports that lysosomal acid lipase helps release cholesterol during phagosome maturation. Inhibiting the enzyme changed membrane organisation and had different effects on the survival of two bacterial pathogens.
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Modern gene editing, high-resolution imaging and omics tools have expanded cell biology beyond the two classic forms of cell death. Researchers are also finding that some cells can delay death or recover after a death programme begins.
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A bioRxiv preprint reports that maintaining 10% oxygen throughout human iPSC-cardiomyocyte differentiation favoured atrial rather than ventricular specification. The laboratory finding could help produce atrial cells but raises process-design concerns for manufacturing ventricular cells.
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A bioRxiv preprint reports that the protein PBF/PTTG1IP helps coordinate cell adhesion, front–rear polarity and directional movement. The findings come from mouse fibroblasts and human thyroid cancer cells, making them preclinical mechanistic evidence.
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A bioRxiv preprint identifies phosphatidylinositol (PI) as the preferred direct substrate of the enzyme PLCXD2. In a PLCXD2-deficient retinal model, the loss was associated with altered lipid products, synaptic abnormalities, retinal-layer thinning and weaker electrical responses from photoreceptors.
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A Nature study identifies RNF213 as an enzyme that marks abnormal glycogen, or polyglucosan, for autophagy in brain cells. Experiments in engineered cells and mice link the pathway to protection against polyglucosan accumulation.