7月29日《細胞》（Cell）雜志上周刊登的一項研究提出了減緩甚至扭轉(zhuǎn)衰老過程的新可能性,。
該研究顯示,，動物變老是由遺傳學原因而非組織受損造成的。科學家們傳統(tǒng)上認為，老化是細胞和組織長期磨損和破裂的必然結(jié)果，毒素,、電離輻射、疾病和壓力都會促使動物衰老和死亡,。
現(xiàn)在,，由斯坦福大學的斯圖爾特·金帶領(lǐng)的一個小組，正在對微小的線蟲展開研究,。他們發(fā)現(xiàn),，一種被稱為ELT-3的生物學開關(guān)能夠啟動數(shù)百個涉及老化過程的基因，而當線蟲變老時,，ELT-3變得更加豐富,。
科學家們嘗試人為使這些線蟲變老。他們讓線蟲受到熱和輻射等壓力,，但是這些都不能對涉及老化過程的基因產(chǎn)生影響,。金因此得出結(jié)論：越老的動物，其ELT-3的豐富度越高,，而這是控制機制出錯的結(jié)果,。他稱這種現(xiàn)象為“發(fā)育漂變”。
報道指出,，如果老化不是化學過程造成的災(zāi)難結(jié)果,，而是由于控制它的基因發(fā)生了改變，那么從理論上說,，在任何水平上,，老化速度都可以被減緩甚至停止,。但是金還不能確定,，發(fā)育漂變是否也出現(xiàn)在人類身上。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell,，Vol 134, 291-303,，Yelena V. Budovskaya，Stuart K. Kim
An elt-3/elt-5/elt-6 GATA Transcription Circuit Guides Aging in C. elegans
Yelena V. Budovskaya,1 Kendall Wu,1,3 Lucinda K. Southworth,2 Min Jiang,1 Patricia Tedesco,4 Thomas E. Johnson,4 and Stuart K. Kim1,2,
1 Department of Developmental Biology, Stanford University Medical Center, Stanford, CA 94305, USA
2 Stanford Medical Informatics, Stanford University Medical Center, Stanford, CA 94305, USA
3 Affymetrix, Inc., 3420 Central Expressway, Santa Clara, CA 95051, USA
4 Institute for Behavioral Genetics, Department of Integrative Physiology, University of Colorado, Boulder, Box 447, Boulder, CO 80309, USA
Corresponding author
Stuart K. Kim
[email protected]
Summary
To define the C. elegans aging process at the molecular level, we used DNA microarray experiments to identify a set of 1294 age-regulated genes and found that the GATA transcription factors ELT-3, ELT-5, and ELT-6 are responsible for age regulation of a large fraction of these genes. Expression of elt-5 and elt-6 increases during normal aging, and both of these GATA factors repress expression of elt-3, which shows a corresponding decrease in expression in old worms. elt-3 regulates a large number of downstream genes that change expression in old age, including ugt-9, col-144, and sod-3. elt-5(RNAi) and elt-6(RNAi) worms have extended longevity, indicating that elt-3, elt-5, and elt-6 play an important functional role in the aging process. These results identify a transcriptional circuit that guides the rapid aging process in C. elegans and indicate that this circuit is driven by drift of developmental pathways rather than accumulation of damage.
