This study concludes that moisture migration, caused by an increase in the pore pressure within the material, also causes segregation of the material to occur.
The delay in migration caused by DN-Hub was not due to a disruption of radial glia morphology or the structural integrity of the apical surface, since both appeared normal in electroporated brains (Figure S6A D and not shown).
However, further increases in migration caused the rate of resistance evolution to decline (Fig. 2).
Blockage of single cell migration caused only a small reduction in final ALC diameters in sparse cultures of up to ∼1,500 cells (7.5×104 cells/cm2 in vitro), but had no effect in denser cultures (Fig. 11A).
Conversely, when co-electroporated with shRNA at a 0.5 1 ratio, S404D rSynIII significantly rescued the delay in radial migration caused by SynIII KD at E21. CDK5 is a downstream effector in the Sema3A pathway, and alterations in this pathway at various levels all cause a phenotype similar to SynIII KD in the cortex (Polleux et al., 2000; Behar et al., 1996).
Co-transfection with other miRNAs did not rescue the reduction in cell migration caused by TDP-43 knockdown (Fig. 5A and 5B).
More importantly, forced Tβ10 overexpression completely reversed the promotion of cell migration caused by shRNA silencing of Tβ10 in both the modified Boyden chamber and the monolayer wound healing assays.
LIS1 (PAFAH1B1) mutation can impair neuronal migration, causing lissencephaly in humans.
This layered structure has a major influence on fluid migration, causing flow in high permeability layers to be generally parallel to the direction of bedding, while flow in low permeability layers is perpendicular to bedding (Freeze and Witherspoon 1967).
Failure in neuronal migration causes functional abnormalities in disorders such as Lissencephaly and Zellweger syndrome (Hatten 1999).
