Fig. 4.

Loss of Tsc1 up-regulates cell growth and multiple metabolic programs including glycolysis, mitochondrial respiration, and lipid biosynthesis. (A) Cell size of splenic DCs from spike BM and WT or Tsc1^CreER donor BM-derived cells in the mixed chimeras (generated as described in Fig. 1F). FSC, forward scatter. (B) Size of CD11c⁺ cells derived from 4-OHT–treated WT or Tsc1^CreER total BM cells (Left), LSKs (Center), or MDPs (Right). (C–J) BM cells from WT or Tsc1^CreER mice were cultured with FLT3L and 4-OHT, followed by analysis of CD71 and CD98 expression (C), glycolytic activity through measurement of the generation of ³H₂O from [3-³H]glucose (DPM, disintegrations per minute) (D), extracellular acidification rate (mpH, milli-pH units) (E), mRNA expression of glycolysis-related genes (F), oxygen consumption rate (G), mitochondria mass as determined by MitoTracker Green (H), de novo lipogenesis assay (I), and mRNA expression of lipogenic genes (J). Error bars indicate SEM. Data are representative of two to five independent experiments.