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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Protein-repair and hormone-signaling pathways specify dauer and adult longevity and dauer development in Caenorhabditis elegans.
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Protein-repair and hormone-signaling pathways specify dauer and adult longevity and dauer development in Caenorhabditis elegans.

机译：秀丽隐杆线虫的蛋白质修复和激素信号通路确定了道尔和成年寿命以及道尔的发育。

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摘要

Protein damage that accumulates during aging can be mitigated by a repair methyltransferase, the l-isoaspartyl-O-methyltransferase. In Caenorhabditis elegans, the pcm-1 gene encodes this enzyme. In response to pheromone, we show that pcm-1 mutants form fewer dauer larvae with reduced survival due to loss of the methyltransferase activity. Mutations in daf-2, an insulin/insulin-like growth factor-1-like receptor, and daf-7, a transforming growth factor-beta-like ligand, modulate pcm-1 dauer defects. Additionally, daf-2 and daf-7 mutant dauer larvae live significantly longer than wild type. Although dauer larvae are resistant to many environmental stressors, a proportionately larger decrease in dauer larvae life spans occurred at 25 degrees C compared to 20 degrees C than in adult life span. At 25 degrees C, mutation of the daf-7 or pcm-1 genes does not change adult life span, whereas mutation of the daf-2 gene and overexpression of PCM-1 increases adult life span. Thus, there are both overlapping and distinct mechanisms that specify dauer and adult longevity.
机译：老化过程中积累的蛋白质损伤可以通过修复甲基转移酶（I-异天冬氨酰-O-甲基转移酶）减轻。在秀丽隐杆线虫中，pcm-1基因编码该酶。响应信息素，我们显示pcm-1突变体形成较少的dauer幼虫，由于甲基转移酶活性的丧失而降低了存活率。胰岛素/胰岛素样生长因子-1样受体daf-2和转化生长因子β样配体daf-7的突变可调节pcm-1 dauer缺陷。此外，daf-2和daf-7突变体dauer幼虫的寿命明显长于野生型。尽管道氏幼虫对许多环境胁迫都有抵抗力，但道氏幼虫在25摄氏度下的寿命下降比例则比成人寿命下的20摄氏度成比例更大。在25摄氏度时，daf-7或pcm-1基因的突变不会改变成年寿命，而daf-2基因的突变和PCM-1的过表达会延长成年寿命。因此，既有重叠的机制又有不同的机制来规定dauer和成年人的寿命。

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