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下一代测序的断点作图揭示了携带明显平衡染色体重排的智力缺陷和/或先天性畸形患者的致病基因缺失。

Breakpoint mapping by next generation sequencing reveals causative gene disruption in patients carrying apparently balanced chromosome rearrangements with intellectual deficiency and/or congenital malformations.

机构信息

Laboratoire de Cytogénétique Constitutionnelle, Service de Génétique, Centre de Biologie et de Pathologie Est, 59, boulevard Pinel, BRON 69677 Cedex, France.

出版信息

J Med Genet. 2013 Mar;50(3):144-50. doi: 10.1136/jmedgenet-2012-101351. Epub 2013 Jan 12.

Abstract

BACKGROUND

Apparently balanced chromosomal rearrangements (ABCR) are associated with an abnormal phenotype in 6% of cases. This may be due to cryptic genomic imbalances or to the disruption of genes at the breakpoint. However, breakpoint cloning using conventional methods (ie, fluorescent in situ hybridisation (FISH), Southern blot) is often laborious and time consuming. In this work, we used next generation sequencing (NGS) to locate breakpoints at the molecular level in four patients with multiple congenital abnormalities and/or intellectual deficiency (MCA/ID) who were carrying ABCR (one translocation, one complex chromosomal rearrangement and two inversions), which corresponded to nine breakpoints.

METHODS

Genomic imbalance was previously excluded by array comparative genomic hybridisation (CGH) in all four patients. Whole genome paired-end protocol was used to identify breakpoints. The results were verified by FISH and by PCR with Sanger sequencing.

RESULTS

We were able to map all nine breakpoints. NGS revealed an additional breakpoint due to a cryptic inversion at a breakpoint junction in one patient. Nine of 10 breakpoints occurred in repetitive elements and five genes were disrupted in their intronic sequence (TCF4, SHANK2, PPFIA1, RAB19, KCNQ1).

CONCLUSIONS

NGS is a powerful tool allowing rapid breakpoint cloning of ABCR at the molecular level. We showed that in three out of four patients, gene disruption could account for the phenotype, allowing adapted genetic counselling and stopping unnecessary investigations. We propose that patients carrying ABCR with an abnormal phenotype should be explored systematically by NGS once a genomic imbalance has been excluded by array CGH.

摘要

背景

显然平衡的染色体重排 (ABCR) 在 6%的病例中与异常表型相关。这可能是由于隐匿性基因组失衡或断裂点处基因的破坏所致。然而,使用传统方法(即荧光原位杂交 (FISH)、Southern 印迹)进行断裂点克隆通常既费力又费时。在这项工作中,我们使用下一代测序 (NGS) 在携带 ABCR(一次易位、一次复杂染色体重排和两次倒位)的四名多发性先天异常和/或智力缺陷 (MCA/ID) 患者中在分子水平定位断裂点,这些患者共对应九个断裂点。

方法

在所有四名患者中,之前均通过阵列比较基因组杂交 (CGH) 排除了基因组失衡。全基因组配对末端方案用于识别断裂点。通过 FISH 和 Sanger 测序的 PCR 验证结果。

结果

我们能够定位所有九个断裂点。NGS 在一名患者的断裂点连接处发现了一个隐匿性倒位,从而揭示了另一个断裂点。10 个断裂点中的 9 个发生在重复元件中,5 个基因在其内含子序列中被破坏(TCF4、SHANK2、PPFIA1、RAB19、KCNQ1)。

结论

NGS 是一种强大的工具,可在分子水平上快速克隆 ABCR 的断裂点。我们表明,在四名患者中的三名中,基因破坏可能导致表型,从而进行适应性遗传咨询并停止不必要的调查。我们建议,一旦通过阵列 CGH 排除了基因组失衡,携带异常表型的 ABCR 的患者应通过 NGS 系统地进行探索。

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