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

AMPK activation promotes lipid droplet dispersion on detyrosinated microtubules to increase mitochondrial fatty acid oxidation.
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DOI:
10.1038/ncomms8176
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发表时间:
2015-05-27
影响因子:
16.6
通讯作者:
Pol, Albert
Pol, Albert
中科院分区:
综合性期刊1区
文献类型:
--
作者:
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

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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. Lipid droplets (LDs) supply fatty acids to cellular processes and move bidirectionally on microtubules. Here the authors show that nutrient starvation causes dispersal of mitochondria and LD to the periphery of the cell along detyrosinated microtubules and increases LD–mitochondria interactions in an AMPK-dependent manner.
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