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. 2016 Dec 14;25(2):216–221. doi: 10.1038/ejhg.2016.145

Figure 4.

Figure 4

Epilepsy-causing missense SIK1 sequence variation associated with increased proximal neurite branching and increased neurite number. Sholl analysis of neurite branching in neurons infected at 14 weeks and expressing wild-type or mutant SIK1 (a–e; bar=100 μm) revealed significantly increased proximal intersections in neurons expressing the missense mutant p.(Pro287Thr; 5.1 intersections vs 3.7 intersections; *P=0.01). The kinase-dead control sequence variant p.(Lys56Met) neurons showed significantly fewer proximal intersections (2.7 intersections vs 3.7 intersections; **P=0.003). No significant differences in intersection number were observed in neurons expressing the truncating SIK1 sequence variants p.(Glu347*) or p.(Gln633*). Neurons expressing the missense p.(Pro287Thr) SIK1 sequence variant also had significantly increased total neurite number (g; *P=0.016), increased primary neurite number (h; *P=0.046) and secondary neurite number (i; *P=0.022) compared with wild type. In contrast, neurons expressing the kinase-dead p.(Lys56Met) SIK1 sequence variant had overall decreased numbers of total neurites (g; **P=0.005) and primary neurites (h; **P=0.004). No significant differences in neurite number were observed in neurons expressing the truncating SIK1 sequence variants.