Department of Bioengineering and Therapeutic Sciences and 2Institute for Human Genetics, University of California-San Francisco, CA, USA.
Hum Mol Genet. 2012 Nov 15;21(22):4930-8. doi: 10.1093/hmg/dds336. Epub 2012 Aug 21.
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.
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。