Fig. 6
From: Genetic interaction of DISC1 and Neurexin in the development of fruit fly glutamatergic synapses
Suppression of DNRX1 with deletion/mutation DISC1 constructs. a DISC1 protein domains and the structure of the deletion/mutation constructs. NLS nuclear localization signal, SF Ser-Phe rich domain, NES nuclear exclusion signal, LZ leucine-zipper domain. Representative interacting proteins are shown above the structure. PDE4 phosphodiesterase type 4, GSK3β glycogen synthase kinase 3β, TNIK TRAF2 and NCK-interacting protein kinase, KAL7 kalirin 7, ATF4 activating transcription factor 4, LIS1 lissencephaly protein 1, NDE1 nuclear distribution protein nudE homolog 1, NDEL1 nuclear distribution protein nudE-like 1. b–g) Representative confocal images of NMJs immunostained with anti-HRP (green) and anti-DNRX1 (magenta) antibodies. The deletion/mutation DISC1 proteins were driven by tubP-GAL4. h Quantification of DNRX1 expression level in the muscle 6/7 boutons normalized to HRP immunoreactivity. Comparisons are against FL (1–854). Note that both 1–402 and 291–854 caused DNRX1 suppression as did FL (1–854) (control vs. FL (1–402), p = 0.0001; control vs. 291–854, p = 0.0108, by Dunnett’s post hoc test). i Quantification of HRP immunoreactivity in the muscle 6/7 boutons. Data are means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, with one-way ANOVA followed by the Dunnett’s post hoc test. Number of each sample is indicated at the bottom of the bar. The statistical values are listed in Supplementary Table 1
