Chinese scientists have identified a gene playing an important role in regulating the development and lifespan of primates through genome-editing technology and experiments on monkeys and human stem cells.
中国科学家通过基因组编辑技术和猴子及人类干细胞实验，确定了一种在调节灵长类动物发育和寿命方面发挥重要作用的基因。
The study may open the door to new research on human development and aging, as well as new treatments for age-related disorders, said Liu Guanghui, a professor at the Institute of Biophysics of the Chinese Academy of Sciences (CAS).
中国科学院生物物理研究所教授刘光辉称，这项研究可能为人类发展和衰老的新研究以及与年龄相关疾病的新疗法打开了大门。
Understanding the genetic basis of aging is the prerequisite to delaying aging and treating age-related illnesses, Liu said.
刘光辉表示，了解衰老的遗传基础是延缓衰老和治疗与年龄有关的疾病的先决条件。
In 1999, scientists found that the Sir2 gene plays a role in prolonging the lifespan of Saccharomyces cerevisiae, a kind of yeast. Then scientists found that the SIRT6 gene, a homologue of Sir2, is involved in the regulation of aging and longevity in rodents.
1999年，科学家们发现Sir2基因在延长酵母菌的寿命方面起着重要作用。然后科学家们发现，SIRT6基因是Sir2的同源基因，参与了啮齿动物衰老和长寿的调节。
Deficiency of SIRT6 from mice leads to features of accelerated aging such as loss of subcutaneous fat, spinal curvature, colitis and shortening of telomere.
小鼠SIRT6的缺乏导致加速衰老的特征，例如皮下脂肪减少，脊柱弯曲，结肠炎和端粒缩短。

However, the biological function of SIRT6 in primates remains largely unknown.
然而，SIRT6在灵长类动物中的生物学功能仍然很大程度上未知。
A joint research team of scientists from the CAS biophysics and zoology institutes spent three years studying how to knockout SIRT6 gene in different tissues of monkeys using CRISPR-Cas9-based gene editing technology.
由中科院生物物理和动物学研究所的科学家组成的联合研究小组，花了三年时间研究如何利用基于CRISPR-Cas9的基因编辑技术来剔除猴子不同组织中的SIRT6基因。
Scientists injected the gene editing tools into 98 monkey zygotes, of which 48 developed into embryos with normal form and were implanted into 12 surrogate mother monkeys. Four became pregnant, giving birth to three baby monkeys 165 days later and one aborted.
科学家将基因编辑工具注入98只猴子受精卵中，其中48只发育成正常形态的胚胎，并植入12只代孕母猴。四只怀孕，165天后生下三只小猴子，一只流产。
They were the first primates that were deficient in SIRT6 gene. However, different from SIRT6 deficient mice that show premature aging phenomena about two to three weeks after birth, SIRT6-depleted monkeys died within hours after birth. Notably, they exhibited severe prenatal developmental retardation.
它们是第一批SIRT6基因缺失的灵长类动物。然而，与出生后2至3周出现过早衰老现象的SIRT6缺陷小鼠不同，SIRT6耗竭的猴子在出生后数小时内死亡。值得注意的是，它们表现出严重的产前发育迟缓。
"Our results for the first time suggest that SIRT6 is involved in regulating development in non-human primates, and might provide an insight into the research of human developmental disorders," Liu said.
刘光辉说：“我们的结果首次表明SIRT6参与调节非人类灵长类动物的发育，并可能提供对人类发育障碍研究的见解。”
In addition, Chinese scientists conducted in vitro experiments to generate SIRT6-null human embryonic stem cells. This showed that SIRT6 deficiency hindered the differentiation of stem cells to mature neurons.
此外，中国科学家在体外进行了产生SIRT6缺失的人类胚胎干细胞的实验。这表明SIRT6缺乏阻碍了干细胞向成熟神经元的分化。