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No obvious abnormality in mice deficient in receptor protein tyrosine phosphatase beta
S Harroch1, M Palmeri, J Rosenbluth
1Department of Pharmacology and the Skirball Institute, New York University Medical Center, New York, New York 10016, USA.
Abstract:
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 PTPbeta (RPTPbeta; also known as PTPzeta) 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 RPTPbeta 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 RPTPbeta. RPTPbeta-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 RPTPbeta is not essential for neurite outgrowth and node formation in mice. The ultrastructure of nerves of the central nervous system in RPTPbeta-deficient mice suggests a fragility of myelin. However, conduction velocity was not altered in RPTPbeta-deficient mice. The normal development of neurons and glia in RPTPbeta-deficient mice demonstrates that RPTPbeta function is not necessary for these processes in vivo or that loss of RPTPbeta can be compensated for by other PTPs expressed in the nervous system.
Insights
Receptor protein tyrosine phosphatase beta (RPTPbeta) is not essential for neuron and glia development in mice. While RPTPbeta deficiency shows potential myelin fragility, it does not impact nerve conduction or development.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Neuronal and glial development is regulated by extracellular signals influencing protein tyrosine phosphorylation.
- Protein tyrosine phosphatases (PTPs), including receptor PTPbeta (RPTPbeta/PTPzeta), are key regulators in this process.
- RPTPbeta, expressed in the nervous system, has structural similarities to cell adhesion molecules, suggesting a role in cell communication.
Purpose of the Study:
- To investigate the in vivo biological functions of RPTPbeta in the nervous system.
- To determine if RPTPbeta is essential for neuronal migration, neurite outgrowth, and gliogenesis.
- To assess the impact of RPTPbeta deficiency on nervous system development and function.
Main Methods:
- Generation of RPTPbeta-deficient mice.
- Assessment of gross anatomy, nervous system structure, and other organs.
- Evaluation of neurite outgrowth, node formation, and myelin ultrastructure.
- Measurement of nerve conduction velocity.
Main Results:
- RPTPbeta-deficient mice are viable, fertile, and exhibit no gross anatomical abnormalities.
- Contrary to in vitro findings, RPTPbeta is not essential for neurite outgrowth or node formation in vivo.
- Myelin in the central nervous system of deficient mice shows signs of fragility, but nerve conduction velocity remains unaltered.
- Normal development of neurons and glia occurs in the absence of RPTPbeta.
Conclusions:
- RPTPbeta is not essential for the in vivo development of neurons and glia.
- The functions of RPTPbeta in neurite outgrowth and node formation observed in vitro are not critical in vivo.
- Potential compensation by other PTPs may occur, or RPTPbeta's role is less critical than previously hypothesized.
- While myelin fragility is observed, overall nervous system function related to nerve conduction is maintained.
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