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. 2018 Jul 11;9:2679. doi: 10.1038/s41467-018-04990-3

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — CO₂SN/HypSNs systemically control Dilp6 and Serrate. e–g indicate the number of CCs in a single lymph gland lobe. Scale bar: 20μm; except in a, b: 50μm. n.s: not significant (p > 0.01). *p < 0.01; **p < 0.001; ***p < 0.0001. Error bars in c–d and h–l: standard deviation. Bars in graph e–g, x: the median. CO₂SN inhibited conditions: –CO₂R with shaded yellow in f, j–l. Soda-lime generated low CO₂ conditions: shaded blue in d, g. a–d Dilp6 secreted from the fat body is the second systemic signal. dilp6 is expressed upon loss of CO₂SN activity (Gr63a-LexA, LexAop-Shi^ts1; Dilp6-gal4, UAS-GFP) in the fat body (Dilp6, green) (a, b, d), but not the brain or blood (c). e–l dilp6 is necessary and sufficient in extra CC formation. Overexpression of dilp6 in the fat body is sufficient to induce CC differentiation (ppl-gal4; UAS-dilp6) (e). Loss of dilp6 in the fat body reverts CCs in the CO₂SN mutant background to wild-type numbers (Gr63a-LexA, LexAop-Shi^ts1; ppl-gal4, UAS-dilp6^RNAi) (f). This is also seen under soda-lime treatment conditions (ppl-gal4; UAS-dilp6^RNAi) (g). Expression of either upd3 (h) or sima (i) in the brain is sufficient to enhance dilp6 expression in the fat body (Elav-gal4; UAS-upd3 or Elav-gal4; UAS-sima). Increased expression of dilp6 is disrupted by: silencing HypSNs (Gr63a-LexA, LexAop-Shi^ts1; Gyc89da-gal4, UAS-Shi^ts1) (j), by sima RNAi in HypSNs (Gr63a-LexA, LexAop-Shi^ts1; Gyc89da-gal4, UAS-sima^RNAi) (j), upon inhibition of neuronal upd3 (Gr63a-LexA, LexAop-Shi^ts1; Elav-gal4, UAS-upd3^RNAi) (k), or when dome^RNAi is expressed in the fat body (Gr63a-LexA, LexAop-Shi^ts1; ppl-gal4, UAS-dome^RNAi) (l). m–x Insulin receptor (InR) activation by Dilp6 increases Serrate expression. pAKT (pAKT, red) (m–n) and p4EBP (p4EBP, red) (o–p) are upregulated in the lymph gland upon CO₂SN inhibition (Gr63a-gal4; UAS-Gr21a^RNAi). Compared with wild type (q), Serrate expression is substantially enhanced when CO₂SN activity is lost (Gr63a-gal4; UAS-hid,rpr) (Serrate, red) (r). Neuronal expression of either sima (Elav-gal4; UAS-sima) (s) or upd3 (Elav-gal4; UAS-upd3) (t), is sufficient to enhance Serrate protein expression. This phenotype is also seen when dilp6 is overexpressed in the fat body (ppl-gal4; UAS-dilp6) (u). Su(H)-LacZ is activated in cells that receive active Notch signal. The number of such cells increases when CO₂SN activity is attenuated (Gr63a-gal4, Su(H)-LacZ; UAS-hid,rpr) (Su(H)-LacZ, red) (v–w). Quantitation is shown in x