1. Volume 21, Issue 10, Pages 2671-2677 (December 2017)
Opposing Post-transcriptional Control of InR by FMRP and LIN-28 Adjusts Stem Cell- Based Tissue Growth 
Arthur Luhur, Kasun Buddika, Ishara Surangi Ariyapala, Shengyao Chen, Nicholas Samuel Sokol 
Cell Reports 
Volume 21, Issue 10, Pages (December 2017)
DOI: /j.celrep
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2. Cell Reports 2017 21, 2671-2677DOI: (10.1016/j.celrep.2017.11.039)
Copyright © 2017 The Author(s) Terms and Conditions

3. Figure 1
fmr1 Limits the Expansion of the Intestinal Progenitor Cell Population
(A) Intestines stained for LIN-28::Venus (green), FMRP (red), and DNA (blue). Scale bar, 50 μm.
(B) Intestinal progenitors stained for EB reporter gbe-LacZ (white), LIN-28::Venus (green), FMRP (red), and DNA (blue). Scale bar, 3 μm.
(C) Control and fmr1Δ50m/Δ113m mutant intestines stained for progenitor marker esg-LacZ (green) and DNA (blue). Areas used to quantify gut width (arrowheads) and progenitor number (boxes) are shown. Scale bar, 100 μm.
(D) Line plots of progenitor numbers in the posterior midguts of control, fmr1Δ50m/Δ113m mutant, lin-28Δ1 mutant, or lin-28Δ1, fmr1Δ50m/Δ113m double mutant at eclosion as well as 1, 4, and 11 days thereafter. Error bars indicate 95% confidence interval (CI).
(E) Number of mitotic pH3+ cells per control (+/+), fmr1Δ50m/Δ113m (−/−), or rescuedΔ50m/Δ113m (r/−) posterior midgut at 4 and 10 days after eclosion.
(F) Percentages of asymmetric and symmetric divisions in control (+/+), fmr1Δ50m/Δ113m (−/−), and rescuedΔ50m/Δ113m (r/−) posterior midgut at 4 and 10 days after eclosion.
(G) Numbers of esg+ progenitor cells per control (+/+), fmr1Δ50m/Δ113m (−/−), or rescuedΔ50m/Δ113m (r/−) posterior midgut of 6- to 7-day-old females. (D–G) Significance of control versus mutant comparisons as well as numbers of samples are indicated, except for (D) where numbers of samples are listed in the Experimental Procedures. See also Figure S1.
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4. Figure 2 fmr1 Regulates Insulin Signaling via lin-28
(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; InRDf(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 the Experimental Procedures. See also Figure S2.
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5. Figure 3 fmr1 and lin-28 Have Opposing Effects on InR Levels
(A) InR::V5 construction scheme. See the Experimental Procedures for a full description. Inset: PCR-based confirmation of InR tagging is shown.
(B) Intestinal progenitors from esgTS (control), esgTS/UAS-fmr1, and esgTS/UAS-lin-28 intestines stained for esg>GFP (green), InR::V5 (red), and DNA (blue). Scale bar, 3 μm.
(C) InR::V5 fluorescence intensity of samples shown in (B).
(D) Intestinal progenitors stained for InR::V5 (green), esg-LacZ (red), and DNA (blue) from adults harboring mutations in one or both copies of lin-28 and fmr1. Scale bar, 3 μm.
(E) InR::V5 fluorescence intensity of samples shown in (D). Significance of control versus mutant comparisons as well as numbers of samples are indicated. See also Figure S3.
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6. Figure 4 LIN-28 Is Sensitive to Alterations in fmr1 Dosage
(A) Intestinal progenitors stained for LIN-28::Venus (green) and DNA (blue) from control (left), fmr1Δ50m/Δ113m mutant (middle), and esgTS/UAS-fmr1 (right) intestines. Scale bar, 10 μm.
(B) LIN-28::Venus fluorescence intensity of samples shown in (A). Significance of control versus mutant comparisons as well as numbers of samples are indicated.
(C)Tub-Gal4, UAS-gfp-labeled adult control (left), fmr1Δ50m (middle), and UAS-fmr1 (right) clones generated in 7-day-old adults and stained for GFP (green), LIN-28::mCherry (red), and DNA (blue). Scale bar, 3 μm.
(D) In our model, LIN-28 predominates during adaptive growth to promote the mRNA translation needed for symmetric ISC division and expansion of the progenitor population. FMRP is activated later, during the transition from growth to homeostasis, in order to recruit LIN-28-repressive mRNPs and switch the ISC division pattern from symmetric to asymmetric. See also Figure S4.
Cell Reports  , DOI: ( /j.celrep )
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