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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Mice deficient in the chemokine receptor CXCR4 exhibit impaired limb innervation and myogenesis.

The chemokine CXCL12/SDF-1 and its receptor CXCR4 regulate the development and the function of the hematopoietic system and control morphogenesis of distinct brain areas. Here, we demonstrate that inactivation of CXCR4 results in a massive loss of spinal cord motoneurons and dorsal root ganglion neurons and, subsequently, in a reduced innervation of the developing mouse fore- and hindlimbs. However, only the death of sensory neurons seems to be a direct consequence of receptor inactivation as suggested by the observations that DRG neurons, but not motoneurons, of wild-type animals express CXCR4 and respond to CXCL12 with an increase in cell survival. In contrast, the increased death of motoneurons in CXCR4-deficient animals seems to result from impaired limb myogenesis and a subsequent loss of muscle-derived neurotrophic support. In summary, our findings unravel a previously unrecognized complex role of CXCL12/CXCR4 in the control of limb neuromuscular development.[1]

References

  1. Mice deficient in the chemokine receptor CXCR4 exhibit impaired limb innervation and myogenesis. Odemis, V., Lamp, E., Pezeshki, G., Moepps, B., Schilling, K., Gierschik, P., Littman, D.R., Engele, J. Mol. Cell. Neurosci. (2005) [Pubmed]
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