Arking R
Exp Gerontol. 1987;22(3):199-220. doi: 10.1016/0531-5565(87)90040-4.
Long lived strains of Drosophila melanogaster have been generated via 25 generations of artificial selection. The mean and the maximum lifespans have been increased both absolutely as well as relative to the controls. The mean lifespan of the selected line now exceeds the maximum lifespan of the controls. The data shows that this increase is entirely accounted for by a genetically based delay in the onset of senescence. Identification and analysis of biomarker data involving reproductive functions supports this interpretation and leads to a suggestion of the processes involved in the lifespan extension. This increase in the duration of the pre-senescent period is under both genetic and environmental control. Senescence itself is not under genetic control and appears to occur stochastically. Selection for decreased longevity was unsuccessful, supporting the concept of a minimum species specific lifespan. A testable hypothesis regarding the biphasic mode of gene regulation of senescence is presented in which a gene-environment interaction takes place in larval life that results in a temporal reprogramming of other, presumably structural, genes which act in adult life at a time prior to the onset of senescence.
通过25代人工选择培育出了寿命较长的黑腹果蝇品系。平均寿命和最长寿命相对于对照在绝对值上都有所增加。所选品系的平均寿命现在超过了对照的最长寿命。数据表明,这种增加完全是由基于遗传的衰老起始延迟所导致的。对涉及生殖功能的生物标志物数据的鉴定和分析支持了这一解释,并提出了寿命延长所涉及的过程。衰老前期持续时间的这种增加受遗传和环境控制。衰老本身不受遗传控制,似乎是随机发生的。选择降低寿命的实验未成功,这支持了物种特定最小寿命的概念。本文提出了一个关于衰老基因调控双相模式的可检验假设,即在幼虫期发生基因 - 环境相互作用,导致其他可能是结构基因的时间重编程,这些基因在成年期衰老开始之前发挥作用。