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首页> 外文期刊>The European Journal of Neuroscience >Huntingtin interacting protein 1 can regulate neurogenesis in Drosophila.
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Huntingtin interacting protein 1 can regulate neurogenesis in Drosophila.

机译：亨廷顿蛋白相互作用蛋白1可以调节果蝇中的神经发生。

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摘要

Huntington's disease (HD) is associated with a range of cellular consequences including selective neuronal death and decreased levels of neurogenesis. Ultimately, these altered processes are dependent upon proteins that interact with Huntingtin (Htt) such as the Huntingtin-interacting protein 1 (Hip1) which has a reduced binding preference to expanded Htt. These effects are similar to those observed with modified Notch signal transduction. As Hip1 plays a key role in endocytosis and intracellular transport, and activation of the Notch signal requires both, we investigated putative links between Hip1 and Notch signaling in flies. We have identified two forms of Hip1 that may be produced through the use of alternative first exons: a version of Hip1 with a lipid-binding ANTH domain and Hip1DeltaANTH lacking this domain. The directed expression of Hip1 decreases, while expression of Hip1DeltaANTH increases, the density of sensory microchaetae on the dorsal notum, a classical model of neurogenesis. A reduction in microchaetae density associated with Notch(Microchaetae Deficient (MCD)) (N(MCD) ) alleles is sensitive to both Hip1 and Hip1DeltaANTH levels, as are the bristle phenotypes generated by misexpression of deltex, a key mediator of Notch signaling. Genetic studies further demonstrate that the observed effects of Hip1 and of Hip1DeltaANTH are sensitive to achaete gene dosage while insensitive to the levels of E(Spl), suggesting a non-canonical Notch neurogenic signal through a deltex-dependent pathway. The novel role we describe for Hip1 in Notch-mediated neurogenesis provides a functional link between Notch signaling and proteins related to HD.
机译：亨廷顿舞蹈病（HD）与一系列细胞后果有关，包括选择性神经元死亡和神经发生水平降低。最终，这些改变的过程取决于与亨廷顿蛋白（Htt）相互作用的蛋白，例如与亨廷顿蛋白相互作用的蛋白1（Hip1），它对扩展的Htt的结合偏好降低。这些效果类似于用改良的Notch信号转导所观察到的效果。由于Hip1在胞吞作用和细胞内转运中起关键作用，并且Notch信号的激活需要两者，因此我们研究了果蝇中Hip1和Notch信号之间的推定联系。我们已经确定了两种形式的Hip1，可以通过使用替代的第一个外显子来产生：具有脂质结合型ANTH结构域的Hip1版本和缺少该结构域的Hip1DeltaANTH。 Hip1的定向表达减少，而Hip1DeltaANTH的表达增加，在背侧背上感觉神经小斑的密度是神经发生的经典模型。与Notch（Microchaetae Deficient（MCD））（N（MCD））等位基因相关的微毛孔密度降低对Hip1和Hip1DeltaANTH水平均敏感，由于delch的错误表达而产生的刷毛表型也是Notch信号传导的关键介体。遗传研究进一步表明，Hip1和Hip1DeltaANTH的观察到的效应对achaete基因剂量敏感，而对E（Spl）的水平不敏感，表明通过deltex依赖性途径的非经典Notch神经源性信号。我们描述的Hip1在Notch介导的神经发生中的新作用提供了Notch信号和与HD相关的蛋白之间的功能联系。

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