Lyle Robert, Béna Frédérique, Gagos Sarantis, Gehrig Corinne, Lopez Gipsy, Schinzel Albert, Lespinasse James, Bottani Armand, Dahoun Sophie, Taine Laurence, Doco-Fenzy Martine, Cornillet-Lefèbvre Pascale, Pelet Anna, Lyonnet Stanislas, Toutain Annick, Colleaux Laurence, Horst Jürgen, Kennerknecht Ingo, Wakamatsu Nobuaki, Descartes Maria, Franklin Judy C, Florentin-Arar Lina, Kitsiou Sophia, Aït Yahya-Graison Emilie, Costantine Maher, Sinet Pierre-Marie, Delabar Jean M, Antonarakis Stylianos E
Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, Switzerland.
Eur J Hum Genet. 2009 Apr;17(4):454-66. doi: 10.1038/ejhg.2008.214. Epub 2008 Nov 12.
Down syndrome (DS) is one of the most frequent congenital birth defects, and the most common genetic cause of mental retardation. In most cases, DS results from the presence of an extra copy of chromosome 21. DS has a complex phenotype, and a major goal of DS research is to identify genotype-phenotype correlations. Cases of partial trisomy 21 and other HSA21 rearrangements associated with DS features could identify genomic regions associated with specific phenotypes. We have developed a BAC array spanning HSA21q and used array comparative genome hybridization (aCGH) to enable high-resolution mapping of pathogenic partial aneuploidies and unbalanced translocations involving HSA21. We report the identification and mapping of 30 pathogenic chromosomal aberrations of HSA21 consisting of 19 partial trisomies and 11 partial monosomies for different segments of HSA21. The breakpoints have been mapped to within approximately 85 kb. The majority of the breakpoints (26 of 30) for the partial aneuploidies map within a 10-Mb region. Our data argue against a single DS critical region. We identify susceptibility regions for 25 phenotypes for DS and 27 regions for monosomy 21. However, most of these regions are still broad, and more cases are needed to narrow down the phenotypic maps to a reasonable number of candidate genomic elements per phenotype.
唐氏综合征(DS)是最常见的先天性出生缺陷之一,也是智力发育迟缓最常见的遗传病因。在大多数情况下,DS是由21号染色体额外拷贝的存在所致。DS具有复杂的表型,DS研究的一个主要目标是确定基因型与表型的相关性。与DS特征相关的21号染色体部分三体和其他人类21号染色体(HSA21)重排病例,可确定与特定表型相关的基因组区域。我们构建了一个覆盖HSA21q的细菌人工染色体(BAC)阵列,并使用阵列比较基因组杂交(aCGH)技术,对涉及HSA21的致病性部分非整倍体和不平衡易位进行高分辨率定位。我们报告了对30个HSA21致病性染色体畸变的鉴定和定位,其中包括19个部分三体和11个HSA21不同区段的部分单体。断点已定位到约85 kb范围内。部分非整倍体的大多数断点(30个中的26个)定位在一个10 Mb的区域内。我们的数据不支持单一的DS关键区域。我们确定了DS 25种表型的易感区域和21号染色体单体的27个区域。然而,这些区域大多仍然较宽泛,需要更多病例才能将表型图谱缩小到每个表型合理数量级的候选基因组元件。