ArticleThe Journal of cell biology2023
Arf1-PI4KIIIβ positive vesicles regulate PI(3)P signaling to facilitate lysosomal tubule fission.
Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Cholesterol maintains the degradative capacity of lysosomes during clearance and recycling of dysfunctional mitochondria.Nature communications · 2026Article
- SEC14L2 couples chaperone-mediated autophagy to microtubule stability by targeting Stathmin 1.Nature communications · 2026Article
- STARD3 regulates lysosome positioning and contacts via a GSK3-controlled phosphorylation switch.The EMBO journal · 2026Article
- Loss of ARF5 impairs recovery after lysosomal damage.Frontiers in molecular biosciences · 2025Article
- Arf1-dependent LRBA recruitment to Rab4 endosomes is required for endolysosome homeostasis.The Journal of cell biology · 2024Article
- Acutely Modifying Phosphatidylinositol Phosphates on Endolysosomes Using Chemically Inducible Dimerization Systems.Bio-protocol · 2024Article
- Mechanisms of lysosomal tubulation and sorting driven by LRRK2.Biochemical Society transactions · 2024Review
- Recombinant biosensors for multiplex and super-resolution imaging of phosphoinositides.The Journal of cell biology · 2024Article
- Reversible assembly and disassembly of V-ATPase during the lysosome regeneration cycle.Molecular biology of the cell · 2024Article
- Article
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Authors and funding
7 authors.
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Abstract
Formation and fission of tubules from autolysosomes, endolysosomes, or phagolysosomes are required for lysosome reformation. However, the mechanisms governing these processes in these different lysosomal organelles are poorly understood. Thus, the role of phosphatidylinositol-4-phosphate (PI(4)P) is unclear as it was shown to promote the formation of tubules from phagolysosomes but was proposed to inhibit tubule formation on autolysosomes because the loss of PI4KIIIβ causes extensive lysosomal tubulation. Using super-resolution live-cell imaging, we show that Arf1-PI4KIIIβ positive vesicles are recruited to tubule fission sites from autolysosomes, endolysosomes, and phagolysosomes. Moreover, we show that PI(4)P is required to form autolysosomal tubules and that increased lysosomal tubulation caused by loss of PI4KIIIβ represents impaired tubule fission. At the site of fission, we propose that Arf1-PI4KIIIβ positive vesicles mediate a PI(3)P signal on lysosomes in a process requiring the lipid transfer protein SEC14L2. Our findings indicate that Arf1-PI4KIIIβ positive vesicles and their regulation of PI(3)P are critical components of the lysosomal tubule fission machinery.
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