Beneficial miscommunication

摘要

不同动物的寿命相差很大，但为什么是这样却rn不清楚。Johan ALmerx及其同事报告了线粒体rn核糖体蛋白表达的自然变化何以能够转化成小rn鼠和蠕虫寿命的延长，并且提出了决定代谢扰rn动对寿命长短的影响的一个统一的机制。在这rn项研究中，他们寻找与近亲繁殖的小鼠的BXDrn基因参照种群中的寿命长短相关的基因变化。%Our existence depends on a small interloper that resides within our cells — the persistent and phantom-like presence of a once autonomous organism. More than 2 billion years ago, as one bacterium tried, but failed, to consume another, two cells forged a relationship that eventually resulted in the evolution of one into a subcellu-lar organelle — the mitochondrion — of the other. As time passed, this organelle became a small metabolic factory for its host cell, allowing the host to produce enough energy I to differentiate and to evolve into the intricate networks of cells and tissues that form the basis of a complex organism~1. What happens to the organism when this endosymbiotic relationship is disrupted, and the surprising effects of this disruption on lifespan,are the focus of a study by Houtkooper et al.~2 on page 451 of this issue.