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. Author manuscript; available in PMC: 2009 Aug 17.
Published in final edited form as: Arch Gen Psychiatry. 2008 Sep;65(9):996–1006. doi: 10.1001/archpsyc.65.9.996

Figure 4. Knockdown of DISC1, BBS4, and PCM1 leads to neuronal migration defects in the developing cerebral cortex.

Figure 4

(A) RNAi constructs and GFP expression vectors were electroporated into the ventricular zone (VZ) at E15 and analyzed at P0. In brains with control RNAi (Con RNAi), 40% of GFP-labeled cells exited the VZ, and 25% of GFP-labeled cells completed migration and formed the superficial layers of the cortex that correspond to bins 9 and 10. By contrast, only less than 15% of GFP-positive cells reached the superficial layers in brain slices with DISC1 RNAi, BBS4 RNAi, or PCM1 RNAi, with the majority of GFP-positive cells remaining in the intermediate zone (IZ), subventricular zone (SVZ), and VZ. Green, cells co-transfected with GFP and RNAi constructs; purple, propidium iodide (PI). Scale bar: 100 µm.

(B) A migration distance is shown. Silencing of DISC1, BBS4, or PCM1 induces delayed radial migration (** P<0.0001). Silencing of both DISC1 and BBS4 expression leads to a more severe defect compared with that with either DISC1 RNAi or BBS4 RNAi. * P<0.05. Values are mean ± SEM.