Researchers find no role for RET-independent GFR-alpha in development or regeneration
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 GFRá-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 GFRá 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 GFRá 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 GFRá is much more widely expressed in the body than is RET and that, in vitro, cells expressing GFRá1 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 GFRá1 signaling plays a significant physiological role in either development or regeneration.
Doug Sipp | EurekAlert!
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