Nat Genet:相同的基因突变,为何只在你身上引发了疾病?

2018-08-22 浮苏 生物探索

8月20日,发表在《Nature Genetics》杂志上一篇报道揭开了导致这一不同现象背后的分子机制:可变外显率(variable penetrance)不同,致病突变突变的严重程度在携带突变的个体之间也不同。同时,研究人员还提供了改变外显率的证据。

8月20日,发表在《Nature Genetics》杂志上一篇报道揭开了导致这一不同现象背后的分子机制:可变外显率(variable penetrance)不同,致病突变突变的严重程度在携带突变的个体之间也不同。同时,研究人员还提供了改变外显率的证据。


来自纽约基因组中心(NYGC)的研究人员和哥伦比亚大学系统生物学系助理教授Tuuli Lappalainen以及Stephane Castel博士共同领导了这项研究。

改变外显率假说

外显率,是指在一个群体有致病基因的个体中,表现出相应病理表型人数的百分率。

长期以来,可变外显率一直是预测疾病严重程度的一个挑战,即使对那些具有强遗传关联的疾病也是如此。对此,Lappalainen博士及其同事提出了改变外显率假说——他们认为调控基因激活的基因突变也可以在改变同一基因的编码突变的外显率方面发挥作用。

作为改变外显率假说的首次测试,研究人员对基因型-组织表达(GTEx)项目的数据进行了分析,该项目是影响人类基因表达的一大类基因突变,目的是评估在没有严重遗传疾病的人群中调控和编码突变之间的相互作用。



该研究举例说明了单个个体对于调节突变和致病编码突变都是杂合的。这两种可能的单倍型构型将导致编码突变的外显率降低(如果它在低表达的单倍型上),或增加(如果它在高表达的单倍型上)。来源: NYGC

他们发现,通过降低与疾病发展相关的编码突变的外显率,调节和编码突变的组合得到了丰富,这种组合被称为单倍型,通过降低编码突变的外显率来起到预防疾病的作用。Castel博士解释说,这一发现在普通人群中属于意料之中,因为随着时间的推移,自然选择从基因组中去除了有害的基因突变。

为了在特定疾病的患者群体中验证这一假设,研究人员分析了来自美国国家卫生研究院的癌症基因组图谱( TCGA )和Simons Simplex Collection(SSC,目前世界上最大最严格定义的自闭症数据库之一),在癌症患者和孤独症患者中,他们发现单倍型的富集可以分别增加与癌症和自闭症谱系障碍相关的编码突变的外显率。

CRISPR / Cas9验证

最后,作者们利用CRISPR / Cas9技术设计了一个实验,用已知与疾病相关的编码突变来测试修正的外显率假说。他们选择了一种与Birt-hog-Dube综合征(一种罕见的常染色体显性遗传卵泡刺激素基因异常性疾病)相关的编码突变,通过将SNP编辑成不同单倍型的细胞系,并带有一个调控突变,研究人员能够证明,调控突变确实改变了编码致病突变的效果,这与基于大规模数据收集的预期一致。这一发现为科学家进一步测试特定疾病SNPs提供了一个重要的框架,以确定它们是否会受到改良外显率的影响。

总结来说,在这项研究中,作者们提供了改变外显率的证据。在外显率中,控制基因活动的基因突变修改了由蛋白质编码基因突变引起的疾病风险。该研究将改良的外显率与全基因组水平的特定疾病联系起来,这对于未来预测癌症和自闭症等严重疾病的严重程度具有令人兴奋的意义。

未来计划

Lappalainen博士说:“现在我们已经证明了一种改变外显率的机制,这项研究的长期目标是通过整合调控和编码突变,更好地预测一个人是否会有疾病。”

“将来,对严重疾病遗传原因的研究应该将调控突变与编码突变一起考虑,这将有助人们对与疾病相关的编码突变 风险有一个更细致的理解。” Castel博士补充道。

原始出处:

Stephane E. Castel, Alejandra Cervera, Pejman Mohammadi, et.al. Modified penetrance of coding variants by cis-regulatory variation contributes to disease risk. Nature Genetics (2018)

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    2019-01-20 canlab
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    2019-06-29 cy0324
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    2019-04-08 liye789132251
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    2018-08-24 易水河

    这是个问题啊

    0

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    2018-08-22 清风拂面

    谢谢分享学习

    0

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