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bendless a Drosophila gene affecting neuronal connectivity encodes a ubiquitin-conjugating enzyme homolog

机译:无弯果蝇基因影响神经元连接编码泛素结合酶同源物。

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摘要

The Drosophila bendless (ben) gene was originally isolated as a mutation affecting the escape jump response. This behavioral defect was ascribed to a single lesion affecting the connectivity between the giant fiber and the tergotrochanter motor neuron. A closer examination of the ben phenotype suggests that ben activity is broader and affects a variety of other neurons including photoreceptor cells and their axons. Mosaic analysis indicates that the focus of ben activity is presynaptic. We have cloned the ben gene through a chromosomal walk and show that it is homologous to a class of ubiquitin-conjugating enzymes. The major role of ubiquitination in the protein degradative pathway suggests that ben regulates neural developmental processes such as growth cone guidance by targeting specific proteins for degradation.
机译:果蝇弯曲(ben)基因最初是作为影响逃逸跳跃反应的突变而分离的。这种行为缺陷归因于单个病变,影响了巨纤维和三角肌运动神经元之间的连通性。对苯表型的仔细检查表明,苯的活性范围更广,并影响多种其他神经元,包括感光细胞及其轴突。镶嵌分析表明,ben活动的焦点是突触前。我们已经通过染色体游走克隆了ben基因,并表明它与一类泛素结合酶同源。泛素化在蛋白质降解途径中的主要作用表明,ben通过靶向降解特定的蛋白质来调节神经发育过程,例如生长锥的引导。

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