Caenorhabditis elegans 的 lifespan 被各种各样的基因、环境的因素决定。在这篇论文, spr-3, C。elegans 哺乳动物的神经限制 silencing 因素(NRSF/REST ) 的相应基因,被报导是调整 C 的 lifespan 的重要基因。elegans。spr-3, spr-3 (ok2525 ) ,或 spr-3 表示的 RNAi 抑制的一个删除变化在 C 导致了短 lifespan 显型。elegans。然而, spr-3 的一个胡说八道变化, spr-3 (by108 ) ,增加了 lifespan 26% 什么时候与野类型的线虫的相比。spr-3 (by108 ) 也显示出增加的抵抗到环境应力。spr-3 (by108 ) 变异基因编码 C 终端有与 REST4 可比较的结构的截断的蛋白质, NRSF/REST 在的 splice 变体哺乳动物。spr-3 (by108 ) 的长 lifespan 显型异种在 daf-16 和 glp-1 的正常功能上作为功能和依赖者的获得被证实。spr-3 (by108 ) 的 lifespan 能被在 daf-2 导致一个变化 synergistically 提高。量的聚合酶链反应结果证明 daf-16 以及它的目标基因 sod-3, mtl-1,和 sip-1 的表示在 spr-3 (by108 ) 是起来调整的变异。这些结果将是有用的进一步理解 NRSF/REST 基因的复杂功能在哺乳动物,特别在变老的过程和长寿决心。
The lifespan of Caenorhabditis elegans is determined by various genetic and environmental factors. In this paper, spr-3, a C. elegans homologous gene of the mammalian neural restrictive silencing factor (NRSF/REST), is reported to be an important gene regulating lifespan of C. elegans. A deletion mutation ofspr-3, spr-3(ok2525), or RNAi inhibition of spr-3 expression led to the short lifespan phenotype in C. elegans. However, a nonsense mutation of spr-3, spr-3(by108), increased the lifespan by 26% when compared with that of wild-type nematode. The spr-3(byl08) also showed increased resistance to environmental stress. The spr-3(byl08) mutated gene encodes a C-terminal truncated protein with a structure comparable with the REST4, a splice variant of the NRSF/REST in mammalian. The long lifespan phenotype of spr-3(byl08) mutant is confirmed as a gain of function and dependent on normal functions of daf-16 and glp-1. The lifespan of the spr-3(byl08) can be syner- gistically enhanced by inducing a mutation in daf-2. Quantitative polymerase chain reaction results showed that the expression of daf-16 as well as its target gene sod-3, mtl- 1, and sip-1 was up-regulated in the spr-3(byl08) mutant. These results would be helpful to further understand the complex function of NRSF/REST gene in mammalian, especially in the aging process and longevity determination.