Expression of the Prader-Willi gene Necdin during mouse nervous system development correlates with neuronal differentiation and p75NTR expression.
The expression pattern of Necdin, a gene involved in the etiology of Prader-Willi syndrome and a member of the MAGE family of genes, is described during mouse nervous system development. Using RNA in situ hybridization, immunohistochemical staining, and colocalization with neuronal differentiation markers, we found that Necdin RNA and protein are expressed within post-mitotic neurons at all stages studied. From E10 to E12, Necdin is detected in all developing neurons, in both central and peripheral nervous system, with the highest expression levels in the diencephalon and the hindbrain. After E13, Necdin is expressed in specific structures of the nervous system, in particular the hypothalamus, the thalamus, and the pons, suggesting a specific developmental role therein. In addition, Necdin expression is also detected in non-neural tissues, such as the somites, the developing limb buds, the first branchial arches, the tong, and the axial muscles. Recently, Necdin and other MAGE proteins were found to interact in vitro with the intracellular domain of the p75NTR neurotrophin receptor, but this interaction has not been validated in vivo. We report here that the spatial and temporal expression of p75NTR is included in Necdin expression domain. These results are in agreement with Necdin proposed role on cell cycle arrest, inhibition of apoptosis and facilitation of neuronal differentiation in vitro, and with hypothalamic cellular deficiencies reported in mice with abrogation of the Necdin gene. Furthermore, they are also consistent with the putative role of Necdin in signaling events promoted by p75NTR during mouse nervous system development.
Andrieu
David
D
Neurogenèse et Morphogenèse dans le Développement et chez l'Adulte, CNRS UMR 6156, Institut de Biologie du Développement de Marseille (IBDM), Case 907, Campus de Luminy, 13288 Cedex 9, Marseille, France.
Watrin
Françoise
F
Niinobe
Michio
M
Yoshikawa
Kazuaki
K
Muscatelli
Françoise
F
Fernandez
Pierre Alain
PA
D000818:Animals; D002454:Cell Differentiation; D015870:Gene Expression; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D051379:Mice / Q000196:embryology* / Q000235:genetics / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D009420:Nervous System / Q000033:anatomy & histology / Q000196:embryology* / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D009687:Nuclear Proteins / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D011218:Prader-Willi Syndrome / Q000209:etiology; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000235:genetics / Q000378:metabolism
D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D012333:RNA, Messenger; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; C069766:necdin