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Article

Receptor Protein Tyrosine Phosphatase γ Is a Marker for Pyramidal Cells and Sensory Neurons in the Nervous System and Is Not Necessary for Normal Development

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Pages 5106-5119 | Received 17 Jan 2006, Accepted 15 Apr 2006, Published online: 27 Mar 2023
 

Abstract

In order to gain insight into the biological role of receptor protein tyrosine phosphatase γ (RPTPγ), we have generated RPTPγ-null mice. RPTPγ was disrupted by insertion of the β-galactosidase gene under the control of the RPTPγ promoter. As the RPTPγ-null mice did not exhibit any obvious phenotype, we made use of these mice to study RPTPγ expression and thus shed light on potential biological functions of this phosphatase. Inspection of mouse embryos shows that RPTPγ is expressed in a variety of tissues during embryogenesis. RPTPγ is expressed in both embryonic and adult brains. Specifically, we detected RPTPγ expression in cortical layers II and V and in the stratum pyramidale of the hippocampus, indicating that RPTPγ is a marker for pyramidal neurons. Mixed primary culture of glial cells showed a lack of expression of RPTPγ in astrocytes and a low expression of RPTPγ in oligodendrocytes and in microglia. Interestingly, RPTPγ expression was detected in all sensory organs, including the ear, nose, tongue, eye, and vibrissa follicles, suggesting a potential role of RPTPγ in sensory neurons. An initial behavioral analysis showed minor changes in the RPTPγ-null mice.

We thank Ayala King and Patricia Gaspar for helpful suggestions as well as Muriel Lecocq and Aurore Bugi for excellent technical assistance.

This work was supported by grants to S.H. from the Federation pour la Recherche sur le Cerveau (FRC), l'Association pour la Recherche contre le Cancer (ARC), l'Association pour la Recherche contre la Sclerose en Plaque (ARSEP), GPH-Stem Cells of the Pasteur Institute (Paris, France), and Association Pasteur-Weizmann, as well as by grants from the Ludwig Institute for Cancer Research (to J.S.) and the NIH (RO1-AR051448 and RO1-AR051886 to J.S. and P50-MH066392 to J.D.B.). S. Lamprianou is a recipient of a fellowship from the French Ministry. N. Vacaresse was a recipient of an ELA (European Association against Leucodystrophy) fellowship.

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