Fig. 6: mTORC1 induces NMUR1 expression through an epigenetic mechanism.

a, b Seahorse analysis of the extracellular acidification rate (ECAR) (a) (n = 4 for R5/+, n = 3 for R5/+ Rptor^f/f) and oxygen consumption rate (OCR) (b) (n = 8) in lung ILC2s. G, glycolysis; GR, glycolytic reserve; BR, basal respiration; SRC, spare respiratory capacity. c Mean fluorescence intensity (MFI) of 2-(N-[7-nitrobenz-2-oxa-1,3-diazol-4-yl] amino) −2-deoxyglucose (2-NBDG) in lung ILC2s (n = 5). d, e MFI of global histone 3 (H3) acetylation at lysins K9 (H3K9ac, n = 5) (d) and K27 (H3k27ac, n = 6) (e). f Quantification of H3K27 acetylation at the NMUR1 promoter by ChIP-qPCR in ILC2 from R5/+ and R5/+ Rptor^f/f mice (n = 4 for R5/+, n = 3 for R5/+ Rptor^f/f). g Analysis of citrate concentrations in ILC2s from R5/+ and R5/+ Rptor^f/f mice (n = 4). h, Level of Acetyl-CoA in ILC2s from R5/+ and R5/+ Rptor^f/f mice (n = 6). i Schematic diagram, schematic created in part with BioRender. Shen, L. (2025) https://BioRender.com/udwx3db. j–m Sorted ILC2s were treated with ATP citrate lyase inhibitor (ACLi) (30 μM) (j, k) or Histone Acetyltransferase inhibitor (HATi) (1 μM) (l, m) for 48 h. mRNA expression of Nmur1 (j, l) and relative MFI of NMUR1-Tdtomato (k, m) was determined in ILC2s (n = 4). n, Sorted lung ILC2s from R5/+ and R5/+ Rptor^f/f mice were treated with HATi (1 μM) for 48 h. Expression of NMUR1 in ILC2s was determined by flow cytometry (n = 5). Data were pooled from two independent experiments (a–h, n), and data are representative of two (j–m) independent experiments shown as mean ± SEM. Statistical significance was tested by two-tailed unpaired Student’s t test in (a–m) or two-way ANOVA followed by Tukey’s multiple comparisons test in (n). p-values are shown on the graphs, and p-values < 0.0001 are reported as such. Source data are provided as a Source Data file.