Development 130, e1504 (2003)
Copyright © 2003 The Company of Biologists Limited
CNS development: an engulfing story
Gene inactivation by homologous recombination is a relatively new tool to
become available to the fly community, which Sears et al. have put to good use
on p. 3557 to
inactivate Pvr, which encodes a receptor tyrosine kinase of the
PDGF/VEGF family and is required for hemocyte/macrophage migration. By
examining loss-of-function Pvr mutants, created by both gene
targeting and chemical mutagenesis, the authors have discovered that Pvr is
required for fly CNS morphogenesis – in its absence, axon scaffold
formation and glial mispositioning defects occur in the CNS. By studying two
other fly mutants with similar CNS defects – serpent, which
lacks hemocytes, and flies mutant for the macrophage scavenger receptor,
Croquemort – the authors conclude that the CNS defects of Pvr
mutants are caused by the failure of macrophages to engulf cell corpses within
the CNS, leading to disrupted glial and axon positioning.
Related articles in Development:
- Macrophage-mediated corpse engulfment is required for normal Drosophila CNS morphogenesis
- Heather C. Sears, Caleb J. Kennedy, and Paul A. Garrity
Development 2003 130: 3557-3565.
[Abstract]
[Full Text]
