多細(xì)胞生物的生殖細(xì)胞能實現(xiàn)某種形式的“不朽”：生殖細(xì)胞（卵子或精子）能夠生成它們后代的體細(xì)胞，這些體細(xì)胞在經(jīng)過一定的生長和代謝周期之后會死亡,；但它們也能生成可以傳到下一代的生殖細(xì)胞,。
對線蟲的一系列壽命延長的突變體所做的一項研究顯示，僅僅普通體細(xì)胞,，就可以通過激發(fā)正常情況下只見于“不朽”的生殖細(xì)胞中的基因表達(dá)程序來使壽命延長,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 459, 1079-1084 (25 June 2009) | doi:10.1038/nature08106
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
1 Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
2 Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA
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.
