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The C. elegans LAR-like receptor tyrosine phosphatase PTP-3 and the VAB-1 Eph receptor tyrosine kinase have partly redundant functions in morphogenesis.

机译:秀丽隐杆线虫LAR样受体酪氨酸磷酸酶PTP-3和VAB-1 Eph受体酪氨酸激酶在形态发生中具有部分冗余功能。

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摘要

Receptor-like protein-tyrosine phosphatases (RPTPs) form a diverse family of cell surface molecules whose functions remain poorly understood. The LAR subfamily of RPTPs has been implicated in axon guidance and neural development. Here we report the molecular and genetic analysis of the C. elegans LAR subfamily member PTP-3. PTP-3 isoforms are expressed in many tissues in early embryogenesis, and later become localized to neuronal processes and to epithelial adherens junctions. Loss of function in ptp-3 causes low-penetrance defects in gastrulation and epidermal development similar to those of VAB-1 Eph receptor tyrosine kinase mutants. Loss of function in ptp-3 synergistically enhances phenotypes of mutations in the C. elegans Eph receptor VAB-1 and a subset of its ephrin ligands, but does not show specific interactions with several other RTKs or morphogenetic mutants. The genetic interaction of vab-1 and ptp-3 suggests that LAR-like RPTPs and Eph receptors have related and partly redundant functions in C. elegans morphogenesis.
机译:受体样蛋白酪氨酸磷酸酶(RPTP)形成了细胞表面分子的各种家族,其功能仍知之甚少。 RPTP的LAR亚家族与轴突指导和神经发育有关。在这里,我们报告线虫LAR亚科成员PTP-3的分子和遗传分析。 PTP-3同工型在早期胚胎发生过程中在许多组织中表达,后来定位于神经元过程和上皮粘附连接。与VAB-1 Eph受体酪氨酸激酶突变体相似,ptp-3的功能丧失导致胃排泄和表皮发育中的低渗透性缺陷。 ptp-3中的功能丧失协同增强线虫Eph受体VAB-1及其ephrin配体的一个子集的突变表型,但未显示出与其他几种RTK或形态发生突变体的特异性相互作用。 vab-1和ptp-3的遗传相互作用表明,类似LAR的RPTP和Eph受体在秀丽隐杆线虫形态发生中具有相关的和部分冗余的功能。

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