Nature:“突变”延长寿命?

【字体: 时间:2009年06月29日 来源:生物通

编辑推荐:

  生物通报道,麻省总医院分子生物学,哈佛大学医学院遗传学系的研究者在最新一期的Nature上发表A soma-to-germline transformation in long-lived Caenorhabditis elegans mutants。

  

生物通报道,麻省总医院分子生物学,哈佛大学医学院遗传学系的研究者在最新一期的Nature上发表A soma-to-germline transformation in long-lived Caenorhabditis elegans mutants

 

通讯作者Christian G. RiedelGary Ruvkun是遗传学与RNAi方面的专家,他们一直以秀丽瘾杆线虫为模型研究遗传学与miRNAs方面知识。

 

追求长寿甚至不死一直都是人类的梦想,然后,身体的现实却是,体细胞随着年龄的增长基因组变得越来越不稳定,细胞自我修复的能力也逐渐下降,岁月的手于是在人类身上留下了痕迹,在时间的长河里,人类不断的老去,直至死亡。

 

然而,有一种细胞却具有“不朽”的能力,那就是生殖细胞(精子和卵子),生殖细胞具有自我更新的能力,延续不老的神话。

 

如果,正常的体细胞也能像生殖细胞一样有自我更新的能力,那么是否就能实现不老的梦想。Christian G. RiedelGary Ruvkun等人发现,秀丽瘾杆线虫的体细胞在发生某些突变时能保持体细胞特征不变却同时拥有自我更新能力。

 

当秀丽瘾杆线虫获得这种变异后,体细胞变得更长寿更健康,虫体的寿命也因此延长。

 

如果,有一天这种奇特的突变降临到人类身上,是否也能延长人类的寿命?

(生物通 小茜)

 

生物通推荐原文检索:

A soma-to-germline transformation in long-lived Caenorhabditis elegans mutants

Sean P. Curran1,2, Xiaoyun Wu1,2, Christian G. Riedel1,2 & Gary Ruvkun1,2

 

Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA

Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA

Abstract

Unlike the soma, which ages during the lifespan of multicellular organisms, the germ line traces an essentially immortal lineage. Genomic instability in somatic cells increases with age, and this decline in somatic maintenance might be regulated to facilitate resource reallocation towards reproduction at the expense of cellular senescence. Here we show that Caenorhabditis elegans mutants with increased longevity exhibit a soma-to-germline transformation of gene expression programs normally limited to the germ line. Decreased insulin-like signalling causes the somatic misexpression of the germline-limited pie-1 and pgl family of genes in intestinal and ectodermal tissues. The forkhead boxO1A (FOXO) transcription factor DAF-16, the major transcriptional effector of insulin-like signalling, regulates pie-1 expression by directly binding to the pie-1 promoter. The somatic tissues of insulin-like mutants are more germline-like and protected from genotoxic stress. Gene inactivation of components of the cytosolic chaperonin complex that induce increased longevity also causes somatic misexpression of PGL-1. These results indicate that the acquisition of germline characteristics by the somatic cells of C. elegans mutants with increased longevity contributes to their increased health and survival.

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