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. 2018 Jun 29;9:2548. doi: 10.1038/s41467-018-04882-6

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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. 2 — Neurodevelopmental defects in flies with knockdown of individual 16p11.2 homologs. a Percentage of 16p11.2 homologs with ubiquitous, eye-specific, wing-specific, and pan-neuronal knockdown at various temperatures that manifest specific phenotypes. b Assessment of 16p11.2 homologs for motor defects showed changes in climbing ability over ten days (two-way ANOVA, p = 0.028, df = 62, F = 1.61). Data represented here shows mean ± standard deviation of 10 independent groups of 10 flies for each line. c Assessment of knockdown of 16p11.2 homologs for frequency of spontaneous unprovoked seizure events (n = 5–7 replicate groups of 20 flies each) and average number of seizure events per fly (n = 52–101 individual flies, Mann–Whitney test, *p < 0.05). PPP4C^pp4-19C knockdown was achieved using Elav-GAL4 and no Dicer2, and knockdown of the other two genes and the control used Elav-GAL4 > Dicer2. All boxplots indicate median (center line), 25th and 75th percentiles (bounds of box), and minimum and maximum (whiskers)