Starke Heike, Nietzel Angela, Weise Anja, Heller Anita, Mrasek Kristin, Belitz Britta, Kelbova Christine, Volleth Marianne, Albrecht Beate, Mitulla Beate, Trappe Ralf, Bartels Iris, Adolph Sabine, Dufke Andreas, Singer Sylke, Stumm Markus, Wegner Rolf-Dieter, Seidel Jörg, Schmidt Angela, Kuechler Alma, Schreyer Isolde, Claussen Uwe, von Eggeling Ferdinand, Liehr Thomas
Institut für Humangenetik und Anthropologie, Kollegiengasse 10, 07743 Jena, Germany.
Hum Genet. 2003 Dec;114(1):51-67. doi: 10.1007/s00439-003-1016-3. Epub 2003 Sep 16.
Small supernumerary marker chromosomes (SMCs) are present in about 0.05% of the human population. In approximately 30% of SMC carriers (excluding the approximately 60% SMC derived from one of the acrocentric chromosomes), an abnormal phenotype is observed. The clinical outcome of an SMC is difficult to predict as they can have different phenotypic consequences because of (1). differences in euchromatic DNA-content, (2). different degrees of mosaicism, and/or (3). uniparental disomy (UPD) of the chromosomes homologous to the SMC. Here, we present 35 SMCs, which are derived from all human chromosomes, apart from chromosome 6, as demonstrated by the appropriate molecular cytogenetic approaches, such as centromere-specific multicolor fluoresence in situ hybridization (cenM-FISH), multicolor banding (MCB), and subcentromere-specific multicolor FISH (subcenM-FISH). In nine cases without an aberrant phenotype, neither partial proximal trisomies nor UPD could be detected. Abnormal clinical findings, such as psychomotoric retardation and/or craniofacial dysmorphisms, were associated with seven of the cases in which subcentromeric single-copy probes were proven to be present in three copies. Conversely, in eight cases with a normal phenotype, proximal euchromatic material was detected as partial trisomy. UPD was studied in 12 cases and subsequently detected in two of the cases with SMC (partial UPD 4p and maternal UPD 22 in a der(22)-syndrome patient), indicating that SMC carriers have an enhanced risk for UPD. At present, small proximal trisomies of 1p, 1q, 2p, 6p, 6q, 7q, 9p, and 12q seem to lead to clinical manifestations, whereas partial proximal trisomies of 2q, 3p, 3q, 5q, 7p, 8p, 17p, and 18p may not be associated with significant clinical symptoms. With respect to clinical outcome, a classification of SMCs is proposed that considers molecular genetic and molecular cytogenetic characteristics as demonstrated by presently available methods.
小额外标记染色体(SMCs)在约0.05%的人类群体中存在。在大约30%的SMCs携带者中(不包括约60%源自近端着丝粒染色体之一的SMCs),可观察到异常表型。由于(1)常染色质DNA含量的差异、(2)不同程度的嵌合体以及/或者(3)与SMCs同源的染色体单亲二体(UPD),SMCs的临床结果难以预测。在此,我们展示了35条SMCs,它们源自除6号染色体外的所有人类染色体,这通过适当的分子细胞遗传学方法得以证实,如着丝粒特异性多色荧光原位杂交(cenM-FISH)、多色显带(MCB)以及亚着丝粒特异性多色FISH(subcenM-FISH)。在9例无异常表型的病例中,未检测到部分近端三体或UPD。异常临床发现,如精神运动发育迟缓及/或颅面畸形,与7例病例相关,在这些病例中,亚着丝粒单拷贝探针被证实存在三个拷贝。相反,在8例表型正常的病例中,近端常染色质物质被检测为部分三体。对12例病例进行了UPD研究,随后在2例SMCs病例中检测到UPD(1例der(22)-综合征患者中部分4p UPD和母源22号染色体UPD),表明SMCs携带者发生UPD的风险增加。目前,1p、1q、2p、6p、6q、7q、9p和12q的小近端三体似乎会导致临床表现,而2q、3p、3q、5q、7p、8p、17p和18p的部分近端三体可能与显著的临床症状无关。关于临床结果,提出了一种基于当前可用方法所展示的分子遗传和分子细胞遗传学特征的SMCs分类方法。