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. 2021 Feb 2;10:e58756. doi: 10.7554/eLife.58756

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© 2021, Harrison et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 5. — (A) Overexpressed HA-tagged Kon^ICD in glia (repoGAL4>UASkon^ICD::HA) visualised with anti-HA antibodies in third instar wandering larvae, localises to both glial cytoplasms and nuclei (arrows). (B and C) Overexpression of the intracellular domain of kon (kon^ICD) or dilp-6 increased glial cell number, visualised with repoGAL4>UAShistone-YFP, and quantified automatically with DeadEasy in (C). Overexpression of a dominant negative form of the insulin receptor rescues the increase in cell number caused by Dilp-6 (repo>hisYFP, dilp-6, InRDN), meaning that autocrine InR signalling regulates glial proliferation. Box-plots. One-way ANOVA p<0.0001, post hoc Tukey’s test multiple comparisons between all samples. N = 15–28 ventral nerve cords (VNCs). (D and E) Third star larvae at 72 hr AEL to visualise abdominal developmental neuroblasts: kon-RNAi knock-down in neural stem cells with insGAL4 does not affect Dpn+ cell number. Box-plots. Unpaired Student's t-test, p=0.3111. N = 10 VNCs. (F) Illustration summarising that a positive feedback autocrine loop involving Dilp-6, InR, and Kon promotes both glial proliferation and Dilp-6 production. All images are horizontal views. Asterisks refer to multiple comparison post hoc tests, all samples vs. all: **p<0.01, ****p<0.0001. All graphs show box-plots. For full genotypes and further statistical analysis details, see Supplementary file 1.

Figure 5—figure supplement 1. — (A) Overexpressed HA-tagged Kon^ICD in glia (repoGAL4>UASkon^ICD::HA) visualised with anti-HA antibodies in third instar wandering larvae, localises to both glial cytoplasms and nuclei (arrows). (B and C) Overexpression of the intracellular domain of kon (kon^ICD) or dilp-6 increased glial cell number, visualised with repoGAL4>UAShistone-YFP, and quantified automatically with DeadEasy in (C). Overexpression of a dominant negative form of the insulin receptor rescues the increase in cell number caused by Dilp-6 (repo>hisYFP, dilp-6, InRDN), meaning that autocrine InR signalling regulates glial proliferation. Box-plots. One-way ANOVA p<0.0001, post hoc Tukey’s test multiple comparisons between all samples. N = 15–28 ventral nerve cords (VNCs). (D and E) Third star larvae at 72 hr AEL to visualise abdominal developmental neuroblasts: kon-RNAi knock-down in neural stem cells with insGAL4 does not affect Dpn+ cell number. Box-plots. Unpaired Student's t-test, p=0.3111. N = 10 VNCs. (F) Illustration summarising that a positive feedback autocrine loop involving Dilp-6, InR, and Kon promotes both glial proliferation and Dilp-6 production. All images are horizontal views. Asterisks refer to multiple comparison post hoc tests, all samples vs. all: **p<0.01, ****p<0.0001. All graphs show box-plots. For full genotypes and further statistical analysis details, see Supplementary file 1.