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TRIM9通过DCC和UNC5C控制生长锥对网蛋白的反应。

TRIM9 controls growth cone responses to netrin through DCC and UNC5C.

作者信息

Mutalik Sampada P, O'Shaughnessy Ellen C, Ho Chris T, Gupton Stephanie L

出版信息

bioRxiv. 2024 May 8:2024.05.08.593135. doi: 10.1101/2024.05.08.593135.

Abstract

The guidance cue netrin-1 promotes both growth cone attraction and growth cone repulsion. How netrin-1 elicits these diverse axonal responses, beyond engaging the attractive receptor DCC and repulsive receptors of the UNC5 family, remains elusive. Here we demonstrate that murine netrin-1 induces biphasic axonal responses in cortical neurons: attraction at lower concentrations and repulsion at higher concentrations using both a microfluidic-based netrin-1 gradient and bath application of netrin-1. TRIM9 is a brain-enriched E3 ubiquitin ligase previously shown to bind and cluster the attractive receptor DCC at the plasma membrane and regulate netrin-dependent attractive responses. However, whether TRIM9 also regulated repulsive responses to netrin-1 remained to be seen. In this study, we show that TRIM9 localizes and interacts with both the attractive netrin receptor DCC and the repulsive netrin receptor, UNC5C, and that deletion of murine Trim9 alters both attractive and repulsive responses to murine netrin-1. TRIM9 was required for netrin-1-dependent changes in surface levels of DCC and total levels of UNC5C in the growth cone during morphogenesis. We demonstrate that DCC at the membrane regulates growth cone area and show that TRIM9 negatively regulates FAK activity in the absence of netrin-1. We investigate membrane dynamics of the UNC5C receptor using pH-mScarlet fused to the extracellular domain of UNC5C. Minutes after netrin addition, levels of UNC5C at the plasma membrane drop in a TRIM9-independent fashion, however TRIM9 regulated the mobility of UNC5C in the plasma membrane in the absence of netrin-1. Together this work demonstrates that TRIM9 interacts with and regulates both DCC and UNC5C during attractive and repulsive axonal responses to netrin-1.

摘要

导向信号分子netrin-1既能促进生长锥的吸引,也能促进生长锥的排斥。除了与吸引性受体DCC和UNC5家族的排斥性受体结合外,netrin-1如何引发这些不同的轴突反应仍不清楚。在这里,我们证明了小鼠netrin-1在皮质神经元中诱导双相轴突反应:使用基于微流控的netrin-1梯度和netrin-1的浴应用,在较低浓度下吸引,在较高浓度下排斥。TRIM9是一种在脑中富集的E3泛素连接酶,先前已证明它能在质膜上结合并聚集吸引性受体DCC,并调节netrin依赖性吸引反应。然而,TRIM9是否也调节对netrin-1的排斥反应仍有待观察。在这项研究中,我们表明TRIM9定位于吸引性netrin受体DCC和排斥性netrin受体UNC5C,并与其相互作用,并且删除小鼠Trim9会改变对小鼠netrin-1的吸引和排斥反应。在形态发生过程中,TRIM9是netrin-1依赖性生长锥中DCC表面水平和UNC5C总水平变化所必需的。我们证明膜上的DCC调节生长锥面积,并表明在没有netrin-1的情况下,TRIM9负调节FAK活性。我们使用与UNC5C胞外域融合的pH-mScarlet研究UNC5C受体的膜动力学。添加netrin几分钟后,质膜上UNC5C的水平以不依赖TRIM9的方式下降,然而在没有netrin-1的情况下,TRIM9调节UNC5C在质膜中的流动性。这项工作共同表明,在对netrin-1的吸引和排斥轴突反应过程中,TRIM9与DCC和UNC5C相互作用并对其进行调节。

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