Autophagy-Dependent Shuttling of TBC1D5 Controls Plasma Membrane Translocation of GLUT1 and Glucose Uptake
| العنوان: | Autophagy-Dependent Shuttling of TBC1D5 Controls Plasma Membrane Translocation of GLUT1 and Glucose Uptake |
|---|---|
| المؤلفون: | Jayanta Debnath, Andrew M. Leidal, Srirupa Roy, Jordan Ye, Sabrina M. Ronen |
| المصدر: | Molecular cell, vol 67, iss 1 |
| بيانات النشر: | eScholarship, University of California, 2017. |
| سنة النشر: | 2017 |
| مصطلحات موضوعية: | 0301 basic medicine, Retromer, Glucose uptake, Vesicular Transport Proteins, Autophagy-Related Protein 7, Medical and Health Sciences, Autophagy-Related Protein 5, Mice, Glucose Transporter Type 1, GTPase-Activating Proteins, glycolysis, Biological Sciences, Cell biology, Protein Transport, RNA Interference, Female, retromer, Glycolysis, Microtubule-Associated Proteins, Intracellular, Signal Transduction, autophagy, Endosome, Physiological, Endosomes, Biology, Transfection, Stress, Article, 03 medical and health sciences, Stress, Physiological, Autophagy, Animals, Humans, Molecular Biology, Cell Membrane, Glucose transporter, Autophagosomes, Biological Transport, Cell Biology, Fibroblasts, Autophagic Punctum, carbohydrates (lipids), Retromer complex, Kinetics, 030104 developmental biology, Glucose, HEK293 Cells, biology.protein, GLUT1, Generic health relevance, Lysosomes, Developmental Biology |
| الوصف: | Autophagy traditionally sustains metabolism in stressed cells via promoting intracellular catabolism and nutrient recycling. Here, we demonstrate that in response to stresses requiring increased glycolytic demand, the core autophagy machinery also facilitates glucose uptake and glycolytic flux by promoting cell surface expression of the glucose transporter Glut1/Slc2a1. During metabolic stress, LC3+ autophagic compartments bind and sequester the RabGAP protein TBC1D5 away from its inhibitory interactions with the retromer complex, thereby enabling retromer recruitment to endosome membranes and Glut1 plasma membrane translocation. In contrast, TBC1D5 inhibitory interactions with the retromer are maintained in autophagy-deficient cells, leading to Glut1 mis-sorting into endolysosomal compartments. Furthermore, TBC1D5 depletion in autophagy deficient cells rescues retromer recruitment to endosomal membranes and Glut1 surface recycling. Hence, TBC1D5 shuttling to autophagosomes during metabolic stress facilitates retromer-dependent Glut1 trafficking. Overall, our results illuminate key interconnections between the autophagy and endosomal pathways dictating Glut1 trafficking and extracellular nutrient uptake. |
| وصف الملف: | application/pdf |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cf9713997ec4cf0478b12eb3e21244bcTest https://escholarship.org/uc/item/1h11v9svTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....cf9713997ec4cf0478b12eb3e21244bc |
| قاعدة البيانات: | OpenAIRE |
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