Inhibition of netrin-mediated axon attraction by a receptor protein tyrosine phosphatase
Inhibition of netrin-mediated axon attraction by a receptor protein tyrosine phosphatase
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DOI：
10.1126/science.1096983
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发表时间：
2004-07-02
期刊：
影响因子：
56.9
通讯作者：
Tessier-Lavigne, M
中科院分区：
文献类型：
--
作者：
Chang, C;Yu, TW;Tessier-Lavigne, M
在轴突引导过程中，秀丽隐杆线虫前腹侧微管轴突的腹侧引导由两个线索控制，即由UNC-40/DCC受体识别的UNC-6/netrin引诱剂和由SAX-3/robo受体识别的SLT-1/狭缝驱避剂。我们在此表明，clr-1 中的功能丧失突变增强了 netrin 依赖性吸引力，抑制了 slt-1 突变体的腹侧引导缺陷。 clr-1 编码跨膜受体蛋白酪氨酸磷酸酶 (RPTP)，其在 AVM 中发挥作用，抑制通过 DCC 家族受体 UNC-40 及其效应子 UNC-34/enabled 的信号传导。其他 RPTP 在轴突引导中的已知作用可能是由于 UNC-40/DCC 等引导受体的调节所致。
During axon guidance, the ventral guidance of the Caenorhabditis elegans anterior ventral microtubule axon is controlled by two cues, the UNC-6/ netrin attractant recognized by the UNC-40/DCC receptor and the SLT-1/slit repellent recognized by the SAX-3/robo receptor. We show here that loss-of-function mutations in clr-1 enhance netrin-dependent attraction, suppressing ventral guidance defects in slt-1 mutants. clr-1 encodes a transmembrane receptor protein tyrosine phosphatase ( RPTP) that functions in AVM to inhibit signaling through the DCC family receptor UNC-40 and its effector, UNC-34/enabled. The known effects of other RPTPs in axon guidance could result from modulation of guidance receptors like UNC-40/DCC.