Extended Data Fig. 6: Glycogen pools are altered in the absence of Slc7a11 and affect DC efferocytosis.
From: Targeting SLC7A11 improves efferocytosis by dendritic cells and wound healing in diabetes
a, Schematic of glycogen metabolism pathway indicating the enzymes involved in glycogen breakdown, degradation and synthesis. In box, it is illustrated the inhibitory phosphorylation of Ser641, Ser645 and Ser649 on Gys1 which leads to decreased glycogen synthesis. b, Pygl siRNA targeting in dendritic cells compromises enhanced efferocytosis of Slc7a11-inhibited DCs. Live-cell imaging are expressed as mean ± SEM with n = 4 per condition, and are representative of two independent experiments. *P < 0.05; One-way ANOVA with Tukey’s multiple comparisons test. c, d, PYG inhibition via DAB compromises enhanced efferocytosis of Slc7a11-inhibited (c) or Slc7a11-KO DCs (d). Live-cell imaging are expressed as mean ± SEM with n = 3 per condition, and are representative of two independent experiments. ****P < 0.0001; One-way ANOVA with Tukey’s multiple comparisons test. e, f, Representative immunoblot (e) and quantification of glycogen metabolism enzymes (f). Data are expressed as fold change (FC) of erastin-treated BMDC to DMSO control with n = 14;Pygl and n = 13;Agl, Gys1, pGys1; **P < 0.01; ***P < 0.001, ns: non-significant via paired, two-tailed t-test.
