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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Loss of poly(ADP-ribose) glycohydrolase causes progressive neurodegeneration in Drosophila melanogaster
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Loss of poly(ADP-ribose) glycohydrolase causes progressive neurodegeneration in Drosophila melanogaster

机译：聚（ADP-核糖）糖水解酶的损失导致果蝇黑斑病进行性神经变性

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摘要

Poly(ADP-ribosyl)ation has been suggested to be involved in regulation of DNA repair, transcription, centrosome duplication, and chromosome stability. However, the regulation of degradation of poly(ADP-ribose) and its signif icance are not well understood. Here we report a loss-of-function mutant Drosophila with regard to poly(ADP-ribose) glycohydrolase, a major hydrolyzing enzyme of poly(ADP-ribose). The mutant lacks the conserved catalytic domain of poly(ADP-ribose) glycohydrolase, and exhibits lethality in the larval stages at the normal development temperature of 25℃. However, one-fourth of the mutants progress to the adult stage at 29℃ but showed progressive neurodegeneration with reduced locomotor activity and a short lifespan. In association with this, extensive accumulation of poly(ADP-ribose) could be detected in the central nervous system. These results suggest that poly(ADP-ribose) metabolism is required for maintenance of the normal function of neuronal cells. The phenotypes observed in the parg mutant might be useful to understand neurodegenerative conditions such as the Alzheimer's and Parkinson's diseases that are caused by abnormal accumulation of substances in nervous tissue.
机译：聚（ADP-核糖基）化已被建议参与DNA修复，转录，中心体复制和染色体稳定性的调控。然而，对聚（ADP-核糖）的降解的调控及其意义还没有被很好地理解。在这里，我们报告有关聚（ADP-核糖）糖水解酶，聚（ADP-核糖）的主要水解酶功能丧失的突变果蝇。该突变体缺乏聚（ADP-核糖）糖水解酶的保守催化结构域，在正常发育温度25℃时，其幼虫期具有致死性。然而，四分之一的突变体在29℃时发展到成年期，但表现出进行性神经变性，运动能力降低，寿命短。与此相关，可以在中枢神经系统中检测到聚（ADP-核糖）的大量积累。这些结果表明，聚（ADP-核糖）代谢是维持神经元细胞正常功能所必需的。在parg突变体中观察到的表型可能有助于理解神经退行性疾病，例如由神经组织中异常物质堆积引起的阿尔茨海默氏病和帕金森氏病。

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