Fig. 3 |. 16p11.2 deletion in DR and 5-HT neurons decreases sociability.

a, Schematic of human chromosome 16p11.2 and deletion of syntenic region of mouse chromosome 7F3. b, Genetic crosses used to delete 16p11.2 from whole brain. PND, postnatal day. c, Timeline of experiments. d, e, Quantification of juvenile interaction (d: F_2,30 = 26.98, P < 0.01; n = 8–17) and three-chamber sociability (e: F_2,29 = 10.03, P < 0.001; n = 8–16) in control, heterozygous and homozygous mice with deletion of 16p11.2. f, g, Deletion of 16p11.2 does not alter the novel object interaction assay (f: F_2,31 = 0.6613, P = 0.5233; n = 8–18), but homozygous 16p11.2 deletion increases locomotor activity (g: F_2,27 = 6.341, P < 0.01; n = 7–16). h, Schematic of 16p11.2 deletion in DR. i, Genetic crosses to delete 16p11.2 from 5-HT neurons. j, Timeline of experiments. k, l, Quantification of juvenile interaction (k: F_2,37 = 26.72, P < 0.001; n = 9–16) and three-chamber sociability (l: F_2,23 = 21.45, P < 0.001; n = 8–9) assays in 16p11.2^flx mice expressing ΔCre or Cre in DR and Sert-cre:16p11.2^flx mice. m, n, Deletion of 16p11.2 did not alter the novel object interaction assay (m: F_2,23 = 0.138, P = 0.8718, n = 8–9) or the locomotion assay (n: F_2,22 = 2.371, P = 0.1168, n = 8–9). Data are mean ± s.e.m. **P < 0.01; ***P < 0.001; one-way ANOVA with Tukey’s multiple comparison post hoc test. The schematic of the mouse brain in this figure has been adapted with permission from Franklin & Paxinos⁴⁶.