美国科学家日前通过对芽殖酵母和线虫的基因分析，鉴别出两种生物共有的２５个负责调控寿命长短的基因。
美国华盛顿大学等机构的科学家１３日在《基因组研究》杂志上报告说，在这２５个“长寿基因”中，至少１５个在人的基因组内存在相似版本。这意味着，科学家有可能借此锁定人体内的基因目标，研究如何减缓人的衰老过程，治疗衰老引发的相关疾病。
研究小组人员介绍说，他们选择了单细胞芽殖酵母和秀丽隐杆线虫为基因分析对象，二者都是衰老研究领域常用的模型生物。从进化史来看，这两种生物之间相距大概有１５亿年，如此悬殊的进化差距比小毛虫和人之间的进化距离还要大。
正因如此，从这两种生物体内鉴别出共同拥有的与寿命相关的基因才显得意义重大。另外，人的基因组内也有十几个类似基因存在，这表明，类似基因很可能也能调控人的寿命。
华盛顿大学生物化学家布赖恩·肯尼迪说，他们希望将来通过基因工程方法调控人体内的“长寿基因”，不仅延长人的预期寿命，还能延长“健康寿命”，也就是人的生命中身体健康、不受衰老引起的疾病影响的时间段。
生物谷推荐原始出处:
Genome Research, DOI: 10.1101/gr.074724.107 Published online before print March 13, 2008
Quantitative evidence for conserved longevity pathways between divergent eukaryotic species
Erica D. Smith1,2, Mitsuhiro Tsuchiya1, Lindsay A. Fox1, Nick Dang1, Di Hu1, Emily O. Kerr1, Elijah D. Johnston1, Bie N. Tchao1, Diana N. Pak1, K. Linnea Welton1, Daniel E.L. Promislow3, James H. Thomas4, Matt Kaeberlein2,5, and Brian K. Kennedy1,5
1 Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA; 2 Department of Pathology, University of Washington, Seattle, Washington 98195, USA; 3 Department of Genetics, University of Georgia, Athens, Georgia 30602, USA; 4 Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA
Studies in invertebrate model organisms have been a driving force in aging research, leading to the identification of many genes that influence life span. Few of these genes have been examined in the context of mammalian aging, however, and it remains an open question as to whether and to what extent the pathways that modulate longevity are conserved across different eukaryotic species. Using a comparative functional genomics approach, we have performed the first quantitative analysis of the degree to which longevity genes are conserved between two highly divergent eukaryotic species, the yeast Saccharomyces cerevisiae and the nematode Caenorhabditis elegans. Here, we report the replicative life span phenotypes for single-gene deletions of the yeast orthologs of worm aging genes. We find that 15% of these yeast deletions are long-lived. In contrast, only 3.4% of a random set of deletion mutants are long-lived—a statistically significant difference. These data suggest that genes that modulate aging have been conserved not only in sequence, but also in function, over a billion years of evolution. Among the longevity determining ortholog pairs, we note a substantial enrichment for genes involved in an evolutionarily conserved pathway linking nutrient sensing and protein translation. In addition, we have identified several conserved aging genes that may represent novel longevity pathways. Together, these findings indicate that the genetic component of life span determination is significantly conserved between divergent eukaryotic species, and suggest pathways that are likely to play a similar role in mammalian aging.
