No obvious abnormality in mice deficient in receptor protein tyrosine phosphatase β

The development of neurons and glia is governed by a multitude of extracellular signals that control protein tyrosine phosphorylation, a process regulated by the action of protein tyrosine kinases and protein tyrosine phosphatases (PTPs), Receptor PTP beta (RPTP beta; also known as PTP zeta) is expressed predominantly in the nervous system and exhibits structural features common to cell adhesion proteins, suggesting that this phosphatase participates in cell-cell communication. It has been proposed that the three isoforms of RPTP beta play a role in regulation of neuronal migration, neurite outgrowth, and gliogenesis. To investigate the biological functions of this PTP, we have generated mice deficient in RPTP beta. RPTP beta-deficient mice are viable, are fertile, and showed no gross anatomical alterations in the nervous system or other organs. In contrast to results of in vitro experiments, our study demonstrates that RPTP beta is not essential for neurite outgrowth and node formation in mice, The ultrastructure of nerves of the central nervous system in RPTP beta-deficient mice suggests a fragility of myelin, However, conduction velocity was not altered in RPTP beta-deficient mice. The normal development of neurons and glia in RPTP beta-deficient mice demonstrates that RPTP beta function is not necessary for these processes in vivo or that loss of RPTP beta can be compensated for by other PTPs expressed in the nervous system.