Haemocyte migration was then imaged live for 1 hour post-wounding.
Furthermore, we show that the external environment plays a key role in determining haemocyte migration speeds, potentially by placing spatial constraints on haemocytes that inhibit membrane ruffling.
Tracking haemocyte migration for an hour post-wounding, we found that Ena overexpression increased haemocyte speed towards wounds, whereas inactivation reduced speed compared with wild-type controls (Fig. 3F J; Table 1).
However, despite regulating lamellipodial dynamics similarly, Ena overexpression increased haemocyte migration speeds in vivo, whereas it reduces fibroblast speeds in vitro (Bear et al., 2000).
In light of this apparent paradox we wondered how Ena upregulation in vivo might affect the overall speed of haemocyte migration in a variety of contexts, given that lamellipodial dynamics in haemocytes in vivo seem to be regulated in a similar Ena-dependent manner to fibroblasts in vitro.
Fascin 1 (singed in Drosophila) is important for Drosophila haemocyte migration (Zanet et al., 2009), migration of mature dendritic cells to lymph nodes in mice (Yamakita et al., 2011) and for melanoma tumour cell invasion in 3D Matrigel/collagen matrix (Li et al., 2010).
Integrins are clearly important for haemocyte migration in vivo (Siekhaus et al., 2010; Huelsmann et al., 2006; Urbano et al., 2009), but the nature of adhesions made by these cells has yet to be addressed and Ena-positive, focal-adhesion-like structures do not seem to be present.
FAK plays a central role in mediating cell migration [38], [46], [47].
Concerning EPCs, very little is known in relation to integrins mediating transendothelial migration.
The intracellular cascades mediating proliferation and migration were also significantly affected.
