美國科學(xué)家日前通過對芽殖酵母和線蟲的基因分析,，鑒別出兩種生物共有的２５個負責(zé)調(diào)控壽命長短的基因,。
美國華盛頓大學(xué)等機構(gòu)的科學(xué)家１３日在《基因組研究》雜志上報告說，在這２５個“長壽基因”中,，至少１５個在人的基因組內(nèi)存在相似版本,。這意味著,，科學(xué)家有可能借此鎖定人體內(nèi)的基因目標,，研究如何減緩人的衰老過程，治療衰老引發(fā)的相關(guān)疾病,。
研究小組人員介紹說,，他們選擇了單細胞芽殖酵母和秀麗隱桿線蟲為基因分析對象，二者都是衰老研究領(lǐng)域常用的模型生物,。從進化史來看,，這兩種生物之間相距大概有１５億年，如此懸殊的進化差距比小毛蟲和人之間的進化距離還要大,。
正因如此,，從這兩種生物體內(nèi)鑒別出共同擁有的與壽命相關(guān)的基因才顯得意義重大。另外,，人的基因組內(nèi)也有十幾個類似基因存在,，這表明，類似基因很可能也能調(diào)控人的壽命,。
華盛頓大學(xué)生物化學(xué)家布賴恩·肯尼迪說,，他們希望將來通過基因工程方法調(diào)控人體內(nèi)的“長壽基因”，不僅延長人的預(yù)期壽命,，還能延長“健康壽命”,，也就是人的生命中身體健康、不受衰老引起的疾病影響的時間段,。
生物谷推薦原始出處:
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.
