Palomo-Guerrero, MartaFadó Andrés, RutCasas, MariaPérez-Montero, MartaBaena Muñoz, MiguelHelmer, Patrick ODomínguez, José LuisRoig, AinaSerra i Cucurull, DolorsHayen, HeikoStenmark, HaraldRaiborg, CamillaCasals, Núria2020-03-132020-03-132019-12-232050-084Xhttps://hdl.handle.net/2445/152738Anterograde transport of late endosomes or lysosomes (LE/Lys) is crucial for proper axon growth. However, the role of energetic nutrients has been poorly explored. Malonyl-CoA is a precursor of fatty acids, and its intracellular levels highly fluctuate depending on glucose availability or the energy sensor AMP-activated protein kinase (AMPK). We demonstrate in HeLa cells that carnitine palmitoyltransferase 1C (CPT1C) senses malonyl-CoA and enhances LE/Lys anterograde transport by interacting with the endoplasmic reticulum protein protrudin and facilitating the transfer of Kinesin-1 from protrudin to LE/Lys. In cultured mouse cortical neurons, glucose deprivation, pharmacological activation of AMPK or inhibition of malonyl-CoA synthesis decreases LE/Lys abundance at the axon terminal, and shortens axon length in a CPT1C-dependent manner. These results identify CPT1C as a new regulator of anterograde LE/Lys transport in response to malonyl-CoA changes, and give insight into how axon growth is controlled by nutrients.26 p.application/pdfengcc-by (c) Palomo-Guerrero, Marta et al., 2019http://creativecommons.org/licenses/by/3.0/esCarnitina palmitoïl-transferasa 1AxonsLisosomesCarnitine palmitoyltransferase IAxonsLysosomesinfo:eu-repo/semantics/article6953632020-03-13info:eu-repo/semantics/openAccess31868590