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Fig. 7 | Acta Neuropathologica Communications

Fig. 7

From: Impairment in dynein-mediated nuclear translocation by BICD2 C-terminal truncation leads to neuronal migration defect and human brain malformation

Fig. 7

Schematic diagram depicting the mechanism of BicD2 mutation in neuronal migration defects. As cortical neuron migrates, a swelling first forms within the leading process (a). The centrosome and the entire microtubule network move into the process by dynein pulling on the plus ends of microtubules (b). In the normal condition, BicD2 binds to the NE protein Nesprin-2 and recruits dynein to the nuclear surface. Dynein then engages the plus ends of trailing microtubules and pulls the nucleus forward (c). In BicD2 p.K775X mutant cells, the nuclear recruitment is impaired, resulting in failure of dynein NE localization. This defect prohibits the forward movements of the nucleus in the migrating neuron (b)

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