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- Title
KDEL receptor regulates secretion by lysosome relocation- and autophagy-dependent modulation of lipid-droplet turnover.
- Authors
Tapia, Diego; Jiménez, Tomás; Zamora, Constanza; Espinoza, Javier; Rizzo, Riccardo; González-Cárdenas, Alexis; Fuentes, Danitza; Hernández, Sergio; Cavieres, Viviana A.; Soza, Andrea; Guzmán, Fanny; Arriagada, Gloria; Yuseff, María Isabel; Mardones, Gonzalo A.; Burgos, Patricia V.; Luini, Alberto; González, Alfonso; Cancino, Jorge
- Abstract
Inter-organelle signalling has essential roles in cell physiology encompassing cell metabolism, aging and temporal adaptation to external and internal perturbations. How such signalling coordinates different organelle functions within adaptive responses remains unknown. Membrane traffic is a fundamental process in which membrane fluxes need to be sensed for the adjustment of cellular requirements and homeostasis. Studying endoplasmic reticulum-to-Golgi trafficking, we found that Golgi-based, KDEL receptor-dependent signalling promotes lysosome repositioning to the perinuclear area, involving a complex process intertwined to autophagy, lipid-droplet turnover and Golgi-mediated secretion that engages the microtubule motor protein dynein-LRB1 and the autophagy cargo receptor p62/SQSTM1. This process, here named 'traffic-induced degradation response for secretion' (TIDeRS) discloses a cellular mechanism by which nutrient and membrane sensing machineries cooperate to sustain Golgi-dependent protein secretion. Inter-organelle signaling coordinates adaptive responses via currently unknown mechanisms. Here, Tapia et al. show that KDEL signaling repositions lysosomes in a complex process termed 'traffic-induced degradation response for secretion' (TIDeRS) that connects multiple pathways and Golgi secretion.
- Publication
Nature Communications, 2019, Vol 10, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-019-08501-w