SRF/Mal signaling is essential for border cell migration, as mal mutant cells fail to migrate.
Noteworthy, integrin beta 1 is closely related to primordial germ cell (PGC) migration and mouse PGC lacking integrin beta 1 fail to migrate normally to the gonads [41].
We reasoned that if nhsl1b, vangl2 or scrib mutant FBM neurons fail to migrate in pk1b-depleted hosts, this would mean that the rescue of their migration that we observed in a wild-type environment was mediated by the host FBM neurons themselves.
Without Tbr1, neurons fail to migrate properly.
These findings suggest that conventional optic nerve astrocytes fail to migrate beyond the optic nerve head into the chick retina.
In this context, it has been reported that DCs from CCR7−/− mice fail to migrate into the lymph nodes [3], [5].
In addition, mouse peritoneal exudate cells (PECs) derived from CCR2 deficient (Ccr2−/−) C57BL/6 mice fail to migrate in response to hBD-3 (Joost Oppenheim; personal communication).
Two general models, not necessarily mutually exclusive, could be imagined: progenitor cells are formed in the BM but fail to migrate out into the blood circulation or the cells fail to form in the first place.
Similarly to PLCγ2−/− DCs, Rac1,2−/− DCs fail to migrate in response to CCL21 (Figure 4E) due to impaired CCR7 activation, as ERK phosphorylation in response to CCL21 was significantly dampened in the double KO cells (Figure 4F).
Additionally, our finding as to the increased accumulation of CCR7−/− Treg cells in the lymph nodes was different from the report that transferred CCR7−/− Treg cells fail to migrate into the lymph nodes and suppress antigen-induced T cell response [23].
