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

The development of neurons and glia is governed by a multitude of extracell ular signals that control protein tyrosine phosphorylation, a process regul ated by the action of protein tyrosine kinases and protein tyrosine phospha tases (PTPs), Receptor PTP beta (RPTP beta; also known as PTP zeta) is expr essed predominantly in the nervous system and exhibits structural features common to cell adhesion proteins, suggesting that this phosphatase particip ates in cell-cell communication. It has been proposed that the three isofor ms of RPTP beta play a role in regulation of neuronal migration, neurite ou tgrowth, and gliogenesis. To investigate the biological functions of this P TP, 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 experim ents, our study demonstrates that RPTP beta is not essential for neurite ou tgrowth and node formation in mice, The ultrastructure of nerves of the cen tral nervous system in RPTP beta-deficient mice suggests a fragility of mye lin, However, conduction velocity was not altered in RPTP beta-deficient mi ce. The normal development of neurons and glia in RPTP beta-deficient mice demonstrates that RPTP beta function is not necessary for these processes i n vivo or that loss of RPTP beta can be compensated for by other PTPs expre ssed in the nervous system.