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. 2017 Dec 28;10:62. doi: 10.1186/s13041-017-0342-7

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Loss of presynaptic gef26 function leads to synaptic overgrowth at the NMJ. a Confocal images of anti-HRP-labeled NMJs 6/7 (left) and NMJs 4 (right) in wild-type (w ¹¹¹⁸) and gef26 ⁶/Df third-instar larvae. gef26 mutant NMJs have increased numbers of total and satellite boutons compared with wild type. Arrowheads mark satellite boutons. Scale bars, 20 μm. b Quantification of total bouton number normalized to muscle surface area and satellite bouton number at NMJ 6/7 and NMJ 4 in wild-type, gef26 ⁶/gef26 ⁶, gef26 ⁶/Df, C155-GAL4/+; gef26 ⁶/Df; UAS-gef26/+ (Gef26 rescue-pre), and gef26 ⁶/Df; BG57-GAL4/UAS-gef26 (Gef26 rescue-post) third-instar larvae. The number of NMJs analyzed is indicated in each bar. Data are expressed as mean ± SEM. All comparisons are made with wild-type (*P < 0.001)