On May 5, 2016,Molecular Cell published “ULK1/2 Constitute a Bifurcate Node Controlling Glucose Metabolic Fluxes in addition to Autophagy” by Professor Sheng-cai Lin and his team. Their findings are significant to answer whether ULK1/2 may act as a multi-branching node connecting nutritional stress signals to other metabolic pathways, such as the pathways for glucose metabolism. According to their conclusion:
(A) Red blood cells (RBCs) from embryos of different genotypes were extracted and subjected to immunoblotting.
(B) Glucose consumption (left) and ratio of PPP flux versus the direct glycolytic flux (right) of RBCs from embryos of different genotypes placed in complete medium or medium free of amino acid and serum (n= 4 experiments).
(C) Representative ROS level of RBCs from embryos of different genotypes.
(D) Cell lysates of WT MEFs or WT RBCs placed in complete medium or medium free of amino acid and serum for 2hr or treated with 50nM rapamycin for 2hr in complete medium were immunoblotted as indicated.
(E) Weights of the embryos of Ulk+/+Ulk2-/-, Ulk1+/-Ulk2-/-,and Ulk1/2-/- at embryonic day 15.5 (E15.5) from Ulk1+/-Ulk2-/-mouse parents. During the breeding, half of the mice had access to normol water and the other half to water supplemented with 40mM NAC. Only litters containing Ulk1/2-/- embryos were included in the analysis.
(F) Model for Ulk1/2- mediated regulation of glucose metabolic fluxes. Error bars denote SEM Statistical analysis was performed by ANOVA followed by Turkey in (B) and (E) (*p< 0.05;**p<0.01).
Lin and his team from School of Life Sciences focus on the study of molecular mechanisms that underlie metabolic homeostasis and its relationship to cell growth control. In the past three years, a series of their findings have been published in journals like Science, Cell Metabolism, and Molecular Cell.