7月29日《细胞》（Cell）杂志上周刊登的一项研究提出了减缓甚至扭转衰老过程的新可能性。
该研究显示，动物变老是由遗传学原因而非组织受损造成的。科学家们传统上认为，老化是细胞和组织长期磨损和破裂的必然结果，毒素、电离辐射、疾病和压力都会促使动物衰老和死亡。
现在，由斯坦福大学的斯图尔特·金带领的一个小组，正在对微小的线虫展开研究。他们发现，一种被称为ELT-3的生物学开关能够启动数百个涉及老化过程的基因，而当线虫变老时，ELT-3变得更加丰富。
科学家们尝试人为使这些线虫变老。他们让线虫受到热和辐射等压力，但是这些都不能对涉及老化过程的基因产生影响。金因此得出结论：越老的动物，其ELT-3的丰富度越高，而这是控制机制出错的结果。他称这种现象为“发育漂变”。
报道指出，如果老化不是化学过程造成的灾难结果，而是由于控制它的基因发生了改变，那么从理论上说，在任何水平上，老化速度都可以被减缓甚至停止。但是金还不能确定，发育漂变是否也出现在人类身上。（生物谷Bioon.com）
生物谷推荐原始出处：
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
kim@cmgm.stanford.edu
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.
