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 Pvrmutants are caused by the failure of macrophages to engulf cell corpses within the CNS, leading to disrupted glial and axon positioning.
CNS development: an engulfing story
CNS development: an engulfing story. Development 1 August 2003; 130 (15): e1504. doi:
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