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Taken together, Mesp2 can induce mesoderm and EMT in ESCs, and compensate for differentiation and migratory defects in Mesp1-deficient embryos.
Rac1,2−/− DCs have migratory defects in vivo and fail to induce T cell priming due to impaired interactions with T cells [13].
Compensation by other FLN isoforms is a likely explanation for the lack of major migratory defects in most tissues of single knockout animals.
Notably, we observed cell migratory defects in the developing endothelial compartment.
INPP1 inactivation with RNA interference, but not HYI knockdown, led to migratory defects in cancer cells (Supplementary Figure S1B).
This is also in agreement with our previous finding that ectopic expression of the bacterial enzyme IpgD, which converts PI 4,5 P2 into PI5P, at least partly rescues the migratory defects in MTMR3 and PIKfyve siRNA-treated cells., Our previous study and the data presented here, clearly show that PI5P plays a role as a second messenger in cell migration.
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The failure of preplate neurons to polarize in the absence of RELN or SFK signaling could be a consequence of the defects in radial glial morphology previously described in reeler or a secondary consequence of the migratory defects observed in neurons of the reeler ectopic cortical plate.
The migration of YFP+ cells in the absence of Rac3 alone was equivalent to the control animals and this is in line with the fact that no major migratory defects are found in Rac3 mutants (Corbetta et al. 2005).
Alternatively, increased ingested material to process (for instance cholesterol) or other changes in cellular lipid composition/distribution (e.g., phosphoinositides) could underlie migratory defects associated with vacuolation in SCAR mutants.
Therefore, in p35 KOs, interneurons failed to cross the PSB and exhibited a "cortical migratory defect," while in ErbB4 conditional KOs these cells could not advance through the LGE/striatum, thus showing a "GE migratory defect" (see Fig. 5 K).
Besides myospheroid, we have also shown that rhea (talin homologue) and fermitin 1 (kindlin 1 homologue) depleted hemocytes suffer from similar migratory defects, both showing significant decreases in the mean cell speed, a phenotype that has been previously observed in HT-1080 talin-depleted cells in a 3D in vitro assay (Fraley et al., 2010).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com