Neurons depend on external molecular signals for their very survival. These molecules, collectively referred to as neurotrophic factors, include a family of four GDNF Family Ligands (GFLs) that bind to specific receptor sites on the surfaces of neural cells. These sites allow GFLs to signal through a receptor complex composed of the RET tyrosine kinase and a GFR-family receptor. Tyrosine kinases, such as RET, are well-known for their function in phosphorylation cascades that span the cell membrane. The role of the GFR co-receptors in these complexes was long thought to be limited to as a co-receptor for RET, but GFRs have recently been suggested to play other roles as well.

The individual functions of the RET and GFR subunits in these receptor complexes, which are important in developmental milieux from peripheral neurogenesis to the developing kidney, remains a thorny question complicated by the fact that GFR is much more widely expressed in the body than is RET and that, in vitro, cells expressing GFR1 without RET have been shown to respond to GDNF signals. A report by Hideki Enomoto (Team Leader, Laboratory for Neuronal Differentiation and Regeneration) and colleagues at the RIKEN Center for Developmental Biology and the Washington University School of Medicine published in the November 18 issue of Neuron now challenges the view that RET-independent GFR1 signaling plays a significant physiological role in either development or regeneration.

Enomoto first devised an elegant experimental system to make it possible to generate mice specifically lacking RET-independent GFR1. The study of GFR deficiencies in vivo is dogged by the lethality of the phenotype, in which the absence of enteric neurons and functioning kidneys results in death soon after birth. In vitro studies and the proximity of RET-independent GFR and RET-expressing cells in some developmental regions, however, have prompted strong speculation that GFR might be able to operate even in t
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Contact: Doug Sipp
sipp@cdb.riken.jp
RIKEN Center for Developmental Biology
17-Nov-2004

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