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. Author manuscript; available in PMC: 2017 Dec 13.
Published in final edited form as: Cell Rep. 2017 Dec 5;21(10):2671–2677. doi: 10.1016/j.celrep.2017.11.039

Figure 2. fmr1 regulates insulin signaling via lin-28.

Figure 2

(A) Number of esg+, progenitor cells per control, fmr1Δ50m/Δ113m mutant, lin-28Δ1 mutant or lin-28Δ1, fmr1Δ50m/Δ113m double mutant intestine. (B) Membrane intensity of tGPH reporter in control, fmr1Δ50m/Δ113m mutant, lin-28Δ1 mutant and lin-28Δ1, fmr1Δ50m/Δ113m double mutant progenitor cells. (C) Intensity of p-AKT signal in control, fmr1Δ50m/Δ113m mutant, rescued fmr1Δ50m/Δ113m mutant, and lin-28Δ1, fmr1Δ50m/Δ113m double mutant progenitor cells. (D) Number of esg+, progenitor cells per control, fmr1Δ50m/Δ113m mutant, or fmr1Δ50m/Δ113m, chico1/+ mutant intestine. (E) Number of esg+, progenitor cells per control, fmr1Δ50m/Δ113m mutant, fmr1Δ50m/Δ113m; InRE19/+ mutant, or fmr1Δ50m/Δ113m; InR Df(3R)Exel6186/+ mutant intestine. (F) Intensity of p-AKT signal in control and fmr1Δ50m/Δ113m mutant progenitor cells in intestines treated with increasing concentrations of insulin. Error bars indicate SEM. (A-F) Significance of control versus mutant comparisons as well as numbers of samples are indicated except for (F) where numbers of samples are listed in methods section. See also Figure S2.