Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Transmembrane Protein GDE2 Induces Motor Neuron Differentiation in Vivo
Meenakshi Rao and
Shanthini Sockanathan*
During neural development, coordinate regulation of cell-cycleexit and differentiation is essential for cell-fate specification,cell survival, and proper wiring of neuronal circuits. However,the molecules that direct these events remain poorly defined.In the developing spinal cord, the differentiation of motorneuron progenitors into postmitotic motor neurons is regulatedby retinoid signaling. Here, we identify a retinoid-induciblegene, GDE2 (glycerophosphodiester phosphodiesterase 2), encodinga six-transmembrane protein that is necessary and sufficientto drive spinal motor neuron differentiation in vivo. A singleamino acid mutation in the extracellular catalytic domain abolishesprotein function. This reveals a critical role for glycerophosphodiestermetabolism in motor neuron differentiation.
Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.
* To whom correspondence should be addressed. E-mail: ssockan1{at}jhmi.edu
The Developmentally Regulated Osteoblast Phosphodiesterase GDE3 Is Glycerophosphoinositol-specific and Modulates Cell Growth.
D. Corda, T. Kudo, P. Zizza, C. Iurisci, E. Kawai, N. Kato, N. Yanaka, and S. Mariggio (2009)
J. Biol. Chem.
284, 24848-24856
|Abstract »|Full Text »|PDF »
Phosphate and carbon source regulation of two PhoP-dependent glycerophosphodiester phosphodiesterase genes of Streptomyces coelicolor.
F. Santos-Beneit, A. Rodriguez-Garcia, A. K. Apel, and J. F. Martin (2009)
Microbiology
155, 1800-1811
|Abstract »|Full Text »|PDF »
Nolz1 is induced by retinoid signals and controls motoneuron subtype identity through distinct repressor activities.