科學家發現與靈長類動物的生長及壽命有關的關鍵基因

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.

中國科學家通過基因組編輯技術和猴子及人類幹細胞實驗，確定了一種在調節靈長類動物發育和壽命方面發揮重要作用的基因。

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).

中國科學院生物物理研究所教授劉光輝稱，這項研究可能爲人類發展和衰老的新研究以及與年齡相關疾病的新療法打開了大門。

Understanding the genetic basis of aging is the prerequisite to delaying aging and treating age-related illnesses, Liu said.

劉光輝表示，瞭解衰老的遺傳基礎是延緩衰老和治療與年齡有關的疾病的先決條件。

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，科學家們發現Sir2基因在延長酵母菌的壽命方面起着重要作用。然後科學家們發現，SIRT6基因是Sir2的同源基因，參與了齧齒動物衰老和長壽的調節。

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的缺乏導致加速衰老的特徵，例如皮下脂肪減少，脊柱彎曲，結腸炎和端粒縮短。

However, the biological function of SIRT6 in primates remains largely unknown.

然而，SIRT6在靈長類動物中的生物學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動物學研究所的科學家組成的聯合研究小組，花了三年時間研究如何利用基於CRISPR-Cas9的基因編輯技術來剔除猴子不同組織中的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.

科學家將基因編輯工具注入98只猴子受精卵中，其中48只發育成正常形態的胚胎，並植入12只代孕母猴。四隻懷孕，165天后生下三隻小猴子，一隻流產。

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.

它們是第一批SIRT6基因缺失的靈長類動物。然而，與出生後2至3周出現過早衰老現象的SIRT6缺陷小鼠不同，SIRT6耗竭的猴子在出生後數小時內死亡。值得注意的是，它們表現出嚴重的產前發育遲緩。

"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.

劉光輝說：“我們的結果首次表明SIRT6參與調節非人類靈長類動物的發育，並可能提供對人類發育障礙研究的見解。”

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，中國科學家在體外進行了產生SIRT6缺失的人類胚胎幹細胞的實驗。這表明SIRT6缺乏阻礙了幹細胞向成熟神經元的分化。