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本文引用的文献

1
Regulatory variation in a TBX5 enhancer leads to isolated congenital heart disease.调控元件 TBX5 变异导致孤立性先天性心脏病。
Hum Mol Genet. 2012 Jul 15;21(14):3255-63. doi: 10.1093/hmg/dds165. Epub 2012 Apr 27.
2
Coding exons function as tissue-specific enhancers of nearby genes.外显子编码作为附近基因的组织特异性增强子发挥作用。
Genome Res. 2012 Jun;22(6):1059-68. doi: 10.1101/gr.133546.111. Epub 2012 Mar 22.
3
Simple and rapid genetic testing for citrin deficiency by screening 11 prevalent mutations in SLC25A13.通过筛查 SLC25A13 中的 11 种常见突变,实现 citrin 缺陷的简单快速基因检测。
Mol Genet Metab. 2012 Apr;105(4):553-8. doi: 10.1016/j.ymgme.2011.12.024. Epub 2012 Jan 8.
4
Identification of a novel DLX5 mutation in a family with autosomal recessive split hand and foot malformation.在一个常染色体隐性分裂手和足畸形的家族中发现了一个新的 DLX5 突变。
J Med Genet. 2012 Jan;49(1):16-20. doi: 10.1136/jmedgenet-2011-100556. Epub 2011 Nov 25.
5
Downregulation of Dlx5 and Dlx6 expression by Hand2 is essential for initiation of tongue morphogenesis.Hand2 通过下调 Dlx5 和 Dlx6 的表达对于舌形态发生的启动是必需的。
Development. 2011 Jun;138(11):2249-59. doi: 10.1242/dev.056929.
6
cis-regulatory mutations are a genetic cause of human limb malformations.顺式调控基因突变是人类肢体畸形的一种遗传病因。
Dev Dyn. 2011 May;240(5):920-30. doi: 10.1002/dvdy.22535. Epub 2011 Jan 11.
7
Depletion of DSS1 protein disables homologous recombinational repair in human cells.DSS1 蛋白缺失会使人细胞中的同源重组修复失能。
Mutat Res. 2010 Dec 10;694(1-2):60-4. doi: 10.1016/j.mrfmmm.2010.08.007. Epub 2010 Sep 15.
8
Genome-wide profiling of p63 DNA-binding sites identifies an element that regulates gene expression during limb development in the 7q21 SHFM1 locus.全基因组 p63 结合位点分析鉴定出一个调控 7q21 短指畸形 1 (SHFM1)基因座肢体发育过程中基因表达的元件。
PLoS Genet. 2010 Aug 19;6(8):e1001065. doi: 10.1371/journal.pgen.1001065.
9
An SNP in an ultraconserved regulatory element affects Dlx5/Dlx6 regulation in the forebrain.一个单核苷酸多态性(SNP)位于一个超保守调控元件中,影响前脑的 Dlx5/Dlx6 调控。
Development. 2010 Sep;137(18):3089-97. doi: 10.1242/dev.051052. Epub 2010 Aug 11.
10
A systematic approach to identify functional motifs within vertebrate developmental enhancers.一种系统的方法,用于鉴定脊椎动物发育增强子中的功能基序。
Dev Biol. 2010 Jan 15;337(2):484-95. doi: 10.1016/j.ydbio.2009.10.019. Epub 2009 Oct 20.

在 DLX5/6 基因座中对组织特异性增强子进行功能特征分析。

Functional characterization of tissue-specific enhancers in the DLX5/6 locus.

机构信息

Department of Bioengineering and Therapeutic Sciences and 2Institute for Human Genetics, University of California-San Francisco, CA, USA.

出版信息

Hum Mol Genet. 2012 Nov 15;21(22):4930-8. doi: 10.1093/hmg/dds336. Epub 2012 Aug 21.

DOI:10.1093/hmg/dds336
PMID:22914741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3529576/
Abstract

Disruption of distaless homeobox 5 and 6 (Dlx5/6) in mice results in brain, craniofacial, genital, ear and limb defects. In humans, chromosomal aberrations in the DLX5/6 region, some of which do not encompass DLX5/6, are associated with split hand/foot malformation 1 (SHFM1) as well as intellectual disability, craniofacial anomalies and hearing loss, suggesting that the disruption of DLX5/6 regulatory elements could lead to these abnormalities. Here, we characterized enhancers in the DLX5/6 locus whose tissue-specific expression and genomic location along with previously characterized enhancers correlate with phenotypes observed in individuals with chromosomal abnormalities. By analyzing chromosomal aberrations at 7q21, we refined the minimal SHFM1 critical region and used comparative genomics to select 26 evolutionary conserved non-coding sequences in this critical region for zebrafish enhancer assays. Eight of these sequences were shown to function as brain, olfactory bulb, branchial arch, otic vesicle and fin enhancers, recapitulating dlx5a/6a expression. Using a mouse enhancer assay, several of these zebrafish enhancers showed comparable expression patterns in the branchial arch, otic vesicle, forebrain and/or limb at embryonic day 11.5. Examination of the coordinates of various chromosomal rearrangements in conjunction with the genomic location of these tissue-specific enhancers showed a correlation with the observed clinical abnormalities. Our findings suggest that chromosomal abnormalities that disrupt the function of these tissue-specific enhancers could be the cause of SHFM1 and its associated phenotypes. In addition, they highlight specific enhancers in which mutations could lead to non-syndromic hearing loss, craniofacial defects or limb malformations.

摘要

在小鼠中,远端同源盒 5 和 6(Dlx5/6)的缺失会导致脑、颅面、生殖器、耳和肢体缺陷。在人类中,DLX5/6 区域的染色体异常,其中一些不包含 DLX5/6,与分裂手/足畸形 1(SHFM1)以及智力障碍、颅面异常和听力损失有关,这表明 DLX5/6 调节元件的缺失可能导致这些异常。在这里,我们研究了 DLX5/6 基因座中的增强子,其组织特异性表达以及与已鉴定的增强子相关的基因组位置与具有染色体异常的个体中观察到的表型相关。通过分析 7q21 上的染色体异常,我们精确定位了最小的 SHFM1 关键区域,并利用比较基因组学选择了该关键区域中的 26 个进化保守的非编码序列,用于斑马鱼增强子检测。其中 8 个序列被证明可作为脑、嗅球、鳃弓、耳泡和鳍的增强子,重新表达 dlx5a/6a。利用小鼠增强子检测,这些斑马鱼增强子中的几个在胚胎 11.5 天的鳃弓、耳泡、前脑和/或肢体中表现出相似的表达模式。检查各种染色体重排的坐标以及这些组织特异性增强子的基因组位置与观察到的临床异常相关。我们的发现表明,破坏这些组织特异性增强子功能的染色体异常可能是 SHFM1 及其相关表型的原因。此外,它们还突出了特定的增强子,其中突变可能导致非综合征性听力损失、颅面缺陷或肢体畸形。