No obvious abnormality in mice deficient in receptor protein tyrosine phosphatase β
No obvious abnormality in mice deficient in receptor protein tyrosine phosphatase β
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DOI：
10.1128/mcb.20.20.7706-7715.2000
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发表时间：
2000-10-01
影响因子：
5.3
通讯作者：
Schlessinger, J
中科院分区：
文献类型：
--
作者：
Harroch, S;Palmeri, M;Schlessinger, J
神经元和神经胶质细胞的发育受多种细胞外信号支配，这些信号控制蛋白酪氨酸磷酸化，这一过程受蛋白酪氨酸激酶和蛋白酪氨酸磷酸酶（PTP）的作用调节，（RPTP beta;也称为PTP ζ）主要在神经系统中表达并表现出细胞粘附蛋白共有的结构特征，这表明这种磷酸酶参与细胞间的通讯。已经提出RPTP β的三种亚型在神经元迁移、神经突生长和胶质细胞生成的调节中起作用。为了研究这种PTP的生物学功能，我们产生了RPTP β缺陷的小鼠。RPTP β-缺陷小鼠是可行的，是可生育的，并且在神经系统或其他器官中没有显示出大体解剖学改变。与体外实验结果相反，我们的研究表明RPTP β对小鼠神经突起的生长和节点的形成不是必需的。RPTP β缺陷小鼠中枢神经系统的超微结构表明髓鞘的脆性，但传导速度在RPTP β缺陷小鼠中没有改变。RPTP β缺陷小鼠中神经元和神经胶质的正常发育表明，RPTP β功能对于体内这些过程不是必需的，或者RPTP β的损失可以通过神经系统中表达的其他PTP来补偿。
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.