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我科学家首揭灵长类动物发育和寿命调控的关键通路

新华网 2018-08-23 作者:王莹

  

  图为高效制备基因编辑灵长类模型 中科院供图

  记者从中国科学院获悉,该院动物研究所和生物物理研究所的研究团队,结合非人灵长类动物模型、人类干细胞模型及基因编辑技术,首次揭示了可调控灵长类动物出生前发育程序的关键分子开关,首次揭示了灵长类和啮齿类动物在衰老调节通路方面的巨大差异,为开展人类发育和衰老的机制研究奠定了重要基础。该成果于北京时间8月23日在国际学术期刊《自然》上在线发表。

  衰老是人类不可避免的生命阶段,它是机体生理功能随时间逐渐退化的过程,是神经退行性疾病、动脉粥样硬化、糖尿病和恶性肿瘤等慢性疾病的最大风险因素。科研人员介绍,衰老进程由遗传和表观遗传因素共同调控,因此,理解衰老的遗传和表观遗传基础是延缓衰老和防治衰老相关疾病的重要前提。

  早在1999年,人们就发现Sir2基因具有延长酿酒酵母寿命的作用,因此被称为“长寿基因”。在啮齿类动物中,Sir2的同源基因SIRT6也被认为参与了衰老及寿命的调控。据科研人员介绍,过量表达SIRT6能够延长雄性小鼠的寿命,而敲除SIRT6则会使小鼠表现出脊柱弯曲,骨质疏松,肠道上皮受损,端粒缩短等加速衰老的表型,且小鼠寿命缩短至约1个月。

  由于SIRT6在功能上链接着表观遗传稳态、基因组稳定性和代谢调控,因此SIRT6被认为是经典的“长寿蛋白”,并成为人们试图延缓衰老的重要靶标。然而,迄今为止几乎所有SIRT6作为“长寿蛋白”的证据均来源于小鼠和其他低等模式生物,SIRT6能否在灵长类动物中发挥类似的功能尚不清楚。

  在这种情况下,研究团队经过三年的不懈努力,首次实现了SIRT6在非人灵长类动物中的全身敲除,获得了世界上首例特定长寿基因敲除的食蟹猴模型。

  研究发现,与SIRT6敲除小鼠表现的加速衰老表型明显不同,SIRT6敲除的食蟹猴在出生数小时内即死亡。

  多项分析结果显示,SIRT6敲除的食蟹猴未见加速衰老表型,却表现出严重的全身发育迟缓。新生SIRT6敲除猴的脑、肌肉及多种其他器官组织均表现出明显的胚胎期未成熟的细胞和分子特征。

  此外,利用人类干细胞模型开展的研究表明,SIRT6缺乏也可阻滞人类神经干细胞向神经元的分化。

  进一步的分子机制研究发现,SIRT6可以通过介导长链非编码核糖核酸H19印记调控区的组蛋白去乙酰化来反式抑制H19的表达,而SIRT6的缺乏则会在灵长类动物神经前体细胞中引起H19表达的异常上调,进而导致脑发育迟缓。

  此次研究成果有何重大意义?对此,科研人员指出,研究首次结合非人灵长类动物模型、人类干细胞模型及基因编辑技术揭示了可调控灵长类动物出生前发育程序的关键分子开关,为研究人类出生前发育迟缓综合征提供了重要的模型体系。此外,该研究首次揭示了灵长类和啮齿类动物在衰老调节通路方面的巨大差异,为开展人类发育和衰老的机制研究,以及相关疾病的干预奠定了重要的基础。

责任编辑:王超

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