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首页> 外文期刊>Cell cycle >Slug, mammalian homologue gene of Drosophila escargot, promotes neuronal-differentiation through suppression of HEB/daughtherless.
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Slug, mammalian homologue gene of Drosophila escargot, promotes neuronal-differentiation through suppression of HEB/daughtherless.

机译：子弹头，果蝇田螺的哺乳动物同源基因，通过抑制HEB /无雌激素促进神经元分化。

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At the neuron developmental stage, neuron-precursor cells can be differentiated into neuron or glia cells. However, precise molecular mechanism to determine the cell fate has not been clearly demonstrated. In this study, we reveal that Drosophila esgarcot and its mammalian homologue genes, Snail and Slug, play a key role in neuronal differentiation. In Drosophila model system, overexpression of Esg, like as Wingless, suppresses the bristle formation. In contrast, elimination of Esg though RNAi promotes double bristle phenotype. We can also observe the similar phenotype in Snail-overexpression system. In mammalian system, overexpression of Slug or Snail can induce neuronal differentiation. Esg and its mammalian homologue gene Slug directly interact with Daughtherless and its mammalian homologue HEB and eliminate them through siah-1 mediated protein degradation. Thus, overexpression of siah-1 can promote neuron cell differentiation, whereas si-siah-1 blocks the Slug-induced HEB suppression. In fact, Drosophila SINA, Siah-1 homologue, has been also known to be involved in bristle formation and Neuronal differentiation. In addition, it has been revealed that CK1 is involved in Esg or Snail stability and Neuronal differentiation. However, Snail is regulated only by CK1 but not by Siah. Considering the fact that Slug mutations have been found in human genetic disease, waardenberg syndrome, major symptoms of which is loss of hearing neuron and odd eye, our result implies that slug/Snail system is required for proper neuronal differentiation, like as Esg in Drosophila.
机译：在神经元发育阶段，神经元前体细胞可以分化为神经元或神经胶质细胞。但是，尚未明确证明确定细胞命运的精确分子机制。在这项研究中，我们揭示了果蝇esgarcot及其哺乳动物同源基因Snail和Slug在神经元分化中起关键作用。在果蝇模型系统中，Esg的过度表达（如无翅）会抑制刷毛的形成。相反，通过RNAi消除Esg可促进双刷毛表型。我们还可以在Snail过表达系统中观察到相似的表型。在哺乳动物系统中，Slug或Snail的过度表达可诱导神经元分化。 Esg及其哺乳动物同源基因Slug与Daughtherless及其哺乳动物同源HEB直接相互作用，并通过siah-1介导的蛋白质降解消除它们。因此，siah-1的过表达可以促进神经元细胞分化，而si-siah-1则可以阻止Slug诱导的HEB抑制。事实上，果蝇SINA（Siah-1同源物）也被认为与猪鬃的形成和神经元的分化有关。另外，已经揭示CK1参与Esg或Snail的稳定性和神经元分化。但是，Snail仅受CK1调控，而不受Siah调控。考虑到在人类遗传病，waardenberg综合征中发现了Slug突变这一事​​实，其主要症状是听力丧失神经元和奇怪的眼睛，因此我们的结果表明，Slug / Snail系统是适当的神经元分化所必需的，例如果蝇中的Esg 。

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