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Published online 1 May 2006. doi:10.1083/jcb.200508161
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 3, 405-416
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Article

 Distinct mechanisms regulate hemocyte chemotaxis during development and wound healing in Drosophila melanogaster

Will Wood1,2, Celia Faria2, and Antonio Jacinto1,2

1 Instituto Gulbenkian de Ciência, 2780-156 Oeiras, Portugal
2 Instituto de Medicina Molecular, 1649-028 Lisboa, Portugal

Correspondence to Antonio Jacinto: ajacinto{at}fm.ul.pt

Drosophila melanogaster hemocytes are highly motile macrophage-like cells that undergo a stereotypic pattern of migration to populate the whole embryo by late embryogenesis. We demonstrate that the migratory patterns of hemocytes at the embryonic ventral midline are orchestrated by chemotactic signals from the PDGF/VEGF ligands Pvf2 and -3 and that these directed migrations occur independently of phosphoinositide 3-kinase (PI3K) signaling. In contrast, using both laser ablation and a novel wounding assay that allows localized treatment with inhibitory drugs, we show that PI3K is essential for hemocyte chemotaxis toward wounds and that Pvf signals and PDGF/VEGF receptor expression are not required for this rapid chemotactic response. Our results demonstrate that at least two separate mechanisms operate in D. melanogaster embryos to direct hemocyte migration and show that although PI3K is crucial for hemocytes to sense a chemotactic gradient from a wound, it is not required to sense the growth factor signals that coordinate their developmental migrations along the ventral midline during embryogenesis.

Abbreviations used in this paper: CNS, central nervous system; dsRNA, double-stranded RNA; PI3K, phosphoinositide 3-kinase; PIP2, PtdIns(3,4)P2; PIP3, PtdIns(3,4,5)P3; PTEN, phosphatase and tensin homologue; PVR, PDGF/ VEGF receptor.


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