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. 2016 May 5;62(3):359-370.
doi: 10.1016/j.molcel.2016.04.009.

ULK1/2 Constitute a Bifurcate Node Controlling Glucose Metabolic Fluxes in Addition to Autophagy

Terytty Yang Li  1 , Yu Sun  1 , Yu Liang  1 , Qing Liu  1 , Yuzhe Shi  1 , Chen-Song Zhang  1 , Cixiong Zhang  1 , Lintao Song  1 , Pu Zhang  2 , Xianzhong Zhang  2 , Xiaotong Li  1 , Tao Chen  1 , Hui-Ying Huang  1 , Xiadi He  3 , Yi Wang  4 , Yu-Qing Wu  1 , Shaoxuan Chen  1 , Ming Jiang  1 , Canhe Chen  1 , Changchuan Xie  1 , James Y Yang  1 , Yan Lin  3 , Shimin Zhao  3 , Zhiyun Ye  1 , Shu-Yong Lin  1 , Daniel Tsun-Yee Chiu  5 , Sheng-Cai Lin  6
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Free article

ULK1/2 Constitute a Bifurcate Node Controlling Glucose Metabolic Fluxes in Addition to Autophagy

Terytty Yang Li et al. Mol Cell. .
Free article

Abstract

Metabolic reprogramming is fundamental to biological homeostasis, enabling cells to adjust metabolic routes after sensing altered availability of fuels and growth factors. ULK1 and ULK2 represent key integrators that relay metabolic stress signals to the autophagy machinery. Here, we demonstrate that, during deprivation of amino acid and growth factors, ULK1/2 directly phosphorylate key glycolytic enzymes including hexokinase (HK), phosphofructokinase 1 (PFK1), enolase 1 (ENO1), and the gluconeogenic enzyme fructose-1,6-bisphosphatase (FBP1). Phosphorylation of these enzymes leads to enhanced HK activity to sustain glucose uptake but reduced activity of FBP1 to block the gluconeogenic route and reduced activity of PFK1 and ENO1 to moderate drop of glucose-6-phosphate and to repartition more carbon flux to pentose phosphate pathway (PPP), maintaining cellular energy and redox homeostasis at cellular and organismal levels. These results identify ULK1/2 as a bifurcate-signaling node that sustains glucose metabolic fluxes besides initiation of autophagy in response to nutritional deprivation.

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