AMPK activation promotes lipid droplet dispersion on detyrosinated microtubules to increase mitochondrial fatty acid oxidation

Herms, Albert, Bosch, Marta, Reddy, Babu J. N., Schieber, Nicole L., Fajardo, Alba, Ruperez, Celia, Fernandez-Vidal, Andrea, Ferguson, Charles, Rentero, Carles, Tebar, Francesc, Enrich, Carlos, Parton, Robert G., Gross, Steven P. and Pol, Albert (2015) AMPK activation promotes lipid droplet dispersion on detyrosinated microtubules to increase mitochondrial fatty acid oxidation. Nature Communications, 6 7176.1-7176.14. doi:10.1038/ncomms8176


Author Herms, Albert
Bosch, Marta
Reddy, Babu J. N.
Schieber, Nicole L.
Fajardo, Alba
Ruperez, Celia
Fernandez-Vidal, Andrea
Ferguson, Charles
Rentero, Carles
Tebar, Francesc
Enrich, Carlos
Parton, Robert G.
Gross, Steven P.
Pol, Albert
Title AMPK activation promotes lipid droplet dispersion on detyrosinated microtubules to increase mitochondrial fatty acid oxidation
Journal name Nature Communications   Check publisher's open access policy
ISSN 2041-1723
Publication date 2015-05
Sub-type Article (original research)
DOI 10.1038/ncomms8176
Open Access Status DOI
Volume 6
Start page 7176.1
End page 7176.14
Total pages 14
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Collection year 2016
Language eng
Formatted abstract
Lipid droplets (LDs) are intracellular organelles that provide fatty acids (FAs) to cellular processes including synthesis of membranes and production of metabolic energy. While known to move bidirectionally along microtubules (MTs), the role of LD motion and whether it facilitates interaction with other organelles are unclear. Here we show that during nutrient starvation, LDs and mitochondria relocate on detyrosinated MT from the cell centre to adopt a dispersed distribution. In the cell periphery, LD-mitochondria interactions increase and LDs efficiently supply FAs for mitochondrial beta-oxidation. This cellular adaptation requires the activation of the energy sensor AMPK, which in response to starvation simultaneously increases LD motion, reorganizes the network of detyrosinated MTs and activates mitochondria. In conclusion, we describe the existence of a specialized cellular network connecting the cellular energetic status and MT dynamics to coordinate the functioning of LDs and mitochondria during nutrient scarcity.
Keyword Dominant Negative Mutant
Protein Kinase
Intracellular Transport
Nutrient Deprivation
Cell
Phosphorylation
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2016 Collection
Institute for Molecular Bioscience - Publications
Centre for Microscopy and Microanalysis Publications
 
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