原文链接：This broken gene may have turned our ancestors into marathoners—and helped humans conquer the world
发表时间：2018年9月11日
Despite our couch potato lifestyles, long-distance running is in our genes. A new study in mice pinpoints how a stretch of DNA likely turned our ancestors into marathoners, giving us the endurance to conquer territory, evade predators, and eventually dominate the planet.
虽然我们乐于宅在家里，但是长距离奔跑的能力却写在我们基因里的。针对小鼠的最新研究指出很可能正是一个DNA片段让我们的祖先成为了马拉松跑者，并且赋予了人类征服领地，驱赶入侵，最终统治地球所需的耐力。
“This is very convincing evidence,” says Daniel Lieberman, a human evolutionary biologist at Harvard University who was not involved with the work. “It’s a nice piece of the puzzle about how humans came to be so successful.”
哈佛大学人类进化生物学家Daniel Lieberman认为“这是一个很有说服力的证据，它会是解释人类如何变得如此成功的一块重要拼图”。
Human ancestors first distinguished themselves from other primates by their unusual way of hunting prey. Instead of depending on a quick spurt of energy—like a cheetah—they simply outlasted antelopes and other escaping animals, chasing them until they were too exhausted to keep running. This ability would have become especially useful as the climate changed 3 million years ago, and forested areas of Africa dried up and became savannas. Lieberman and others have identified skeletal changes that helped make such long-distance running possible, like longer legs. Others have also proposed that our ancestors’ loss of fur and expansion of sweat glands helped keep these runners cool.
人类祖先最早区别于其他灵长类动物的是他们不同寻常的狩猎方式。并不像猎豹一样依赖瞬时爆发力，他们只是比羚羊或其他逃窜的动物更有耐力，在这些动物无力奔跑时抓住它们。当300万年前气候发生变化，非洲的森林地区由于干旱而变成热带草原时这样的能力更能发挥作用。Lieberman和其他研究者者都认可骨骼的变化例如更长的腿会使长距离奔跑成为可能，也有研究表明皮毛的退化和汗腺的变大也让我们的祖先在奔跑时保持凉爽。
Still, scientists don’t know much about the cellular changes that gave us better endurance, says Herman Pontzer, an evolutionary anthropologist at Duke University in Durham, North Carolina, who was not involved with the work.
根据北卡罗来纳州杜克大学的人类学家Herman Pontzer的观点，科学家对于温度变化是否能够导致耐力的增强仍然并没有过多的了解。
Some clues came 20 years ago, when Ajit Varki, a physician-scientist at the University of California, San Diego (UCSD), and colleagues unearthed one of the first genetic differences between humans and chimps: a gene called CMP-Neu5Ac Hydroxylase(CMAH). Other primates have this gene, which helps build a sugar molecule called sialic acid that sits on cell surfaces. But humans have a broken version of CMAH, so they don’t make this sugar, the team reported. Since then, Varki has implicated sialic acid in inflammation and resistance to malaria.
这项研究的起点在20年前，当时加州大学圣地亚哥分校 (UCSD)的医学科学家Ajit Varki和同事发现了人类和黑猩猩基因的首个不同，被称作CMP-Neu5Ac羟化酶（CMAH）。其他拥有这个基因的灵长类动物将其用来合成位于细胞表面的唾液酸糖分子。但根据研究小组的报告，人类的CMAH基因出现了突变，并没有用来合成糖分子。自那以后Varki开始研究唾液酸对于炎症和对抗疟疾的作用。
In the new study, Varki’s team explored whetherCMAHhas any impact on muscles and running ability, in part because mice bred with a musculardystrophy–likesyndrome get worse when they don’t have this gene. UCSD graduate student Jonathan Okerblom put mice with a normal and broken version ofCMAH(akin to the human version) on small treadmills. UCSD physiologist Ellen Breen closely examined their leg muscles before and after running different distances, some after 2 weeks and some after 1 month.
在这个全新的研究中，Varki的团队探索了CMAH基因对于肌肉和跑步能力的影响，部分原因是当小鼠没有这个基因的时候肌营养不良综合征会变得更加严重。加州大学圣地亚哥分校的毕业生Jonathan Okerblom将具有正常CMAH基因和类似人类的突变CMAH基因的小鼠放在跑步机上，生理学家Ellen Breen对于2周和1个月后小鼠跑动不同距离后的腿部肌肉进行了近距离观察。
After training, the mice with the human version of theCMAHgene ran 12% faster and 20% longer than the other mice, the team reports today in the Proceedings of the Royal Society B. “Nike would pay a lot of money” for that kind of increase in performance in their sponsored athletes, Lieberman says.
在今天发表在英国《皇家学会学报B辑》上，研究团队的研究成果是拥有人类版本的CMAH基因的小鼠比其他小鼠跑步速度快12%，距离长20%。Lieberman表示耐克想要他们赞助的运动员取得这样的成绩增长需要花费不菲。
The team discovered that the “humanized” mice had more tiny blood vessels branching into their leg muscles, and—even when isolated in a dish—the muscles kept contracting much longer than those from the other mice. The humanlike mouse muscles used oxygen more efficiently as well. But the researchers still have no idea how the sugar molecule affects endurance, as it serves many functions in a cell.
研究团队发现模拟人类基因的小鼠有许多分叉到腿部肌肉中的微小血管，与其他小鼠相比肌肉压缩的时间更长，肌肉用氧效率也更高。虽然这类糖分子在细胞中发挥着许多功能，但研究者还不清楚它们是怎样提升耐力的。
Similar improvements probably benefitted our human ancestors, says Andrew Best, a biological anthropology graduate student at the University of Massachusetts (UMass) in Amherst, who was not involved with the work. Varki’s team calculated that this genetic change happened 2 million to 3 million years ago, based on the genetic differences among primates and other animals.
来自马萨诸塞大学阿默斯特分校生物人类学毕业生Andrew Best认为，可能与小鼠相似的提升使得我们的祖先因此而获益。Varki的团队依据灵长类动物和其他动物基因的不同，测算出变化的发生大概在200到300万年前。
That’s “slightly earlier than I’d have expected for such a large shift in [endurance],” says Best, as it predates some of the skeletal modifications, which don’t show up in the fossil record until much later. But to Pontzer, the date makes sense, as these ancestors needed endurance for walking and for digging up food. “Maybe it’s more than about running,” he notes.
Best认为这个推算“比我所预期的耐力发生如此巨大转变的时间要稍早一些”，而且这个时间也比相对更晚之后才出现在化石记录中的骨骼变化要早。但是对于Pontzer来说这样的数据是说得过去的，因为人类的祖先同样需要耐力来行走以及寻找食物，他认为“这些也许比跑步的需要更多”。
However, “Mice are not humans or primates,” says Best’s adviser at UMass, Jason Kamilar, a biological anthropologist also not involved with the new work. “The genetic mechanisms in mice may not necessarily translate to humans or other primates.”
Best在马萨诸塞大学的指导老师生物人类学家Jason Kamilar表示“毕竟小鼠不是人类或者灵长类动物，小鼠的基因机制并能不完全转换到人类或其他灵长类动物身上。”
Either way, says Pontzer, the study is exciting because it gets researchers looking beyond fossils and into what might actually have gone on in the bodies of ancient animals. “This is really energizing work; it tells us how much is out there to do.”
无论如何，Pontzer因为这项研究使研究者的视线从化石转移到古生物体内可能实际发生的事情而感到激动，“这是个令人激励的成果，它告诉了我们还有多少事情要去做。”
