Institute of Biochemistry, Department of Biology, ETH Zürich, Zürich, Switzerland.
Elife. 2017 Dec 28;6:e28329. doi: 10.7554/eLife.28329.
Although individuals of many species inexorably age, a number of observations established that the rate of aging is modulated in response to a variety of mild stresses. Here, we investigated how heat stress promotes longevity in yeast. We show that upon growth at higher temperature, yeast cells relax the retention of DNA circles, which act as aging factors in the mother cell. The enhanced frequency at which circles redistribute to daughter cells was not due to changes of anaphase duration or nuclear shape but solely to the downregulation of the diffusion barrier in the nuclear envelope. This effect depended on the PKA and Tor1 pathways, downstream of stress-response kinase Pkc1. Inhibition of these responses restored barrier function and circle retention and abrogated the effect of heat stress on longevity. Our data indicate that redistribution of aging factors from aged cells to their progeny can be a mechanism for modulating longevity.
虽然许多物种的个体不可避免地会衰老，但有许多观察结果表明，衰老的速度可以通过多种轻度压力来调节。在这里，我们研究了热应激如何促进酵母的长寿。我们发现，在较高温度下生长时，酵母细胞会放松对 DNA 环的保留，这些 DNA 环在母细胞中充当衰老因素。圆形物重新分配到子细胞的频率增加并不是由于后期持续时间或核形状的变化，而仅仅是由于核膜中的扩散屏障下调。这种效应取决于应激反应激酶 Pkc1 下游的 PKA 和 Tor1 途径。抑制这些反应恢复了屏障功能和圆形物的保留，并消除了热应激对长寿的影响。我们的数据表明，衰老因素从衰老细胞向其后代的重新分配可能是调节寿命的一种机制。
