Sun Miao, Li Ning, Dong Wu, Chen Zugen, Liu Qing, Xu Yiming, He Guang, Shi Yongyong, Li Xin, Hao Jiajie, Luo Yang, Shang Dandan, Lv Dan, Ma Fen, Zhang Dai, Hua Rui, Lu Chaoxia, Wen Yaran, Cao Lihua, Irvine Alan D, McLean W H Irwin, Dong Qi, Wang Ming-Rong, Yu Jun, He Lin, Lo Wilson H Y, Zhang Xue
McKusick-Zhang Center for Genetic Medicine and State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Am J Hum Genet. 2009 Jun;84(6):807-13. doi: 10.1016/j.ajhg.2009.04.018. Epub 2009 May 21.
Congenital generalized hypertrichosis terminalis (CGHT) is a rare condition characterized by universal excessive growth of pigmented terminal hairs and often accompanied with gingival hyperplasia. In the present study, we describe three Han Chinese families with autosomal-dominant CGHT and a sporadic case with extreme CGHT and gingival hyperplasia. We first did a genome-wide linkage scan in a large four-generation family. Our parametric multipoint linkage analysis revealed a genetic locus for CGHT on chromosome 17q24.2-q24.3. Further two-point linkage and haplotyping with microsatellite markers from the same chromosome region confirmed the genetic mapping and showed in all the families a microdeletion within the critical region that was present in all affected individuals but not in unaffected family members. We then carried out copy-number analysis with the Affymetrix Genome-Wide Human SNP Array 6.0 and detected genomic microdeletions of different sizes and with different breakpoints in the three families. We validated these microdeletions by real-time quantitative PCR and confirmed their perfect cosegregation with the disease phenotype in the three families. In the sporadic case, however, we found a de novo microduplication. Two-color interphase FISH analysis demonstrated that the duplication was inverted. These copy-number variations (CNVs) shared a common genomic region in which CNV is not reported in the public database and was not detected in our 434 unrelated Han Chinese normal controls. Thus, pathogenic copy-number mutations on 17q24.2-q24.3 are responsible for CGHT with or without gingival hyperplasia. Our work identifies CGHT as a genomic disorder.
先天性全身性终毛增多症(CGHT)是一种罕见病症,其特征为色素性终毛普遍过度生长,且常伴有牙龈增生。在本研究中,我们描述了三个患常染色体显性CGHT的汉族家庭以及一例患有极端CGHT和牙龈增生的散发病例。我们首先在一个大型四代家庭中进行了全基因组连锁扫描。我们的参数多点连锁分析揭示了17号染色体q24.2 - q24.3区域存在CGHT的一个遗传位点。进一步使用来自同一染色体区域的微卫星标记进行两点连锁分析和单倍型分析,证实了该基因定位,并在所有家庭中显示关键区域内存在一个微缺失,所有受影响个体均有此缺失,而未受影响的家庭成员则没有。然后我们使用Affymetrix全基因组人类SNP Array 6.0进行拷贝数分析,在这三个家庭中检测到不同大小和不同断点的基因组微缺失。我们通过实时定量PCR验证了这些微缺失,并证实它们在这三个家庭中与疾病表型完全共分离。然而,在散发病例中,我们发现了一个新生微重复。双色间期荧光原位杂交分析表明该重复是反向的。这些拷贝数变异(CNV)共享一个公共基因组区域,公共数据库中未报告该区域的CNV,且在我们的434名无血缘关系的汉族正常对照中也未检测到。因此,17q24.2 - q24.3上的致病性拷贝数突变是导致伴有或不伴有牙龈增生的CGHT的原因。我们的工作将CGHT确定为一种基因组疾病。