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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Highwire regulates guidance of sister axons in the Drosophila mushroom body.
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Highwire regulates guidance of sister axons in the Drosophila mushroom body.

机译：Highwire调节果蝇蘑菇体内姊妹轴突的引导。

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摘要

Axons often form synaptic contacts with multiple targets by extending branches along different paths. PHR (Pam/Highwire/RPM-1) family ubiquitin ligases are important regulators of axon development, with roles in axon outgrowth, target selection, and synapse formation. Here we report the function of Highwire, the Drosophila member of the PHR family, in promoting the segregation of sister axons during mushroom body (MB) formation. Loss of highwire results in abnormal development of the axonal lobes in the MB, leading to thinned and shortened lobes. The highwire defect is attributable to guidance errors after axon branching, in which sister axons that should target different lobes instead extend together into the same lobe. The highwire mutant MB displays elevation in the level of the MAPKKK Wallenda/DLK (dual leucine zipper kinase), a previously identified substrate of Highwire, and genetic suppression studies show that Wallenda/DLK is required for the highwire MB phenotype. The highwire lobe defect is limited to alpha/beta lobe axons, but transgenic expression of highwire in the pioneering alpha'/beta' neurons rescues the phenotype. Mosaic analysis further shows that alpha/beta axons of highwire mutant clones develop normally, demonstrating a non-cell-autonomous role of Highwire for axon guidance. Genetic interaction studies suggest that Highwire and Plexin A signals may interact to regulate normal morphogenesis of alpha/beta axons.
机译：轴突通常通过沿不同路径延伸分支而与多个目标形成突触接触。 PHR（Pam / Highwire / RPM-1）家族泛素连接酶是轴突发育的重要调节剂，在轴突生长，靶标选择和突触形成中发挥作用。在这里，我们报告了P​​HR家族果蝇成员Highwire在促进蘑菇体（MB）形成过程中姐妹轴突分离方面的功能。高丝的丢失导致MB中轴突叶的异常发育，导致叶变薄和变短。高线缺陷可归因于轴突分支后的引导误差，在这种情况下，应针对不同叶的姊妹轴突一起延伸到同一叶中。 highwire突变体MB显示先前鉴定的Highwire底物MAPKKK Wallenda / DLK（双亮氨酸拉链激酶）水平升高，遗传抑制研究表明，Highwire MB表型需要Wallenda / DLK。高丝叶缺损限于α/β叶轴突，但是在先驱性α'/β'神经元中高丝的转基因表达挽救了表型。镶嵌分析进一步显示，highwire突变体克隆的α/β轴突正常发育，表明Highwire在轴突引导下具有非细胞自主作用。遗传相互作用研究表明，Highwire和Plexin A信号可能相互作用，调节正常的alpha / beta轴突形态。

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