Sentence examples for migration defects led from inspiring English sources

These migration defects led to situations where the posterior basal body was found above the nucleus (Fig. 9Ea) or even between the two nuclei (Fig. 9Eb).

The genetic deletion of Glra2 in our knockout line led to interneuron migration defects, which were restricted to those migrating in the deep SVZ stream.

Nonetheless, other evidence continues to point to roles for FLNs in cell migration: over-expressed FLNa inhibits migration of M2 cells [15] and mouse cortical neurons [21], MEKK4−/− mice exhibit PVH associated with neurons that over-express FLNa and b [21], and a male patient with severe PVH has a FLNa gene duplication [22], suggesting that excess FLNa leads to migration defects.

Using morpholino mediated knockdown experiments, we could demonstrate that the absence of MDGA2A leads to migration defects of trigeminal neurons as well as aberrant axonal growth and defasciculation of facial branchiomotor axons.

Furthermore, genetic disruption of these receptors leads to interneuron migration defects.

In agreement with the above reports, our data indicated that Aip1 deletion resulted in the disruption of E-cadherin distribution in the interface between germ cells and Sertoli cells, which could lead to their migration defects.

Consistent with a role in cell-substrate and/or cell-cell adhesion we had previously shown that triple knockout of all three APP/APLP proteins [ 46] or in utero knockdown of APP/APLPs lead to neuronal migration defects during cortical development [ 45, 46].

Depletion of many of these factors led to distal tip cell migration defects, particularly a failure to stop migrating, a phenotype commonly seen in cacn-1 deficient animals.

The concomitant HSF2-dependent downregulation of multiple MAP genes within fetal cortices exposed to alcohol could therefore block this compensatory mechanism and lead to migration defects.

10.7554/eLife.05279.035 Figure 9. Manipulations of filopodia formation lead to PGC migration defects.

We reasoned that acute ablation of Vangl2 should prevent any compensatory mechanism from arising, and so lead to NC migration defects (Fig. 3I, ii).