Gleghorn Lindsay, Ramesar Rajkumar, Beighton Peter, Wallis Gillian
The Wellcome Trust Centre for Cell-Matrix Research, The University of Manchester, Manchester, United Kingdom.
Am J Hum Genet. 2005 Sep;77(3):484-90. doi: 10.1086/444401. Epub 2005 Jul 22.
Spondyloepiphyseal dysplasia (SED) encompasses a heterogeneous group of disorders characterized by shortening of the trunk and limbs. The autosomal dominant SED type Kimberley (SEDK) is associated with premature degenerative arthropathy and has been previously mapped in a multigenerational family to a novel locus on 15q26.1. This locus contains the gene AGC1, which encodes aggrecan, the core protein of the most abundant proteoglycan of cartilage. We screened AGC1 for mutations and identified a single-base-pair insertion, within the variable repeat region of exon 12 in affected individuals from the family with SEDK, that introduces a frameshift of 212 amino acids, including 22 cysteine residues, followed by a premature stop codon. This is the first identification of an AGC1 mutation causing a human disorder. This finding extends the spectrum of mutated genes that may cause SED and thus will aid in the molecular delineation of this complex group of conditions.
脊椎骨骺发育不良(SED)是一组异质性疾病,其特征为躯干和四肢短小。常染色体显性遗传的金伯利型脊椎骨骺发育不良(SEDK)与过早的退行性关节病相关,此前在一个多代家族中已将其定位到15q26.1上的一个新位点。该位点包含基因AGC1,其编码聚集蛋白聚糖,这是软骨中最丰富的蛋白聚糖的核心蛋白。我们对AGC1进行了突变筛查,在患有SEDK的家族中受影响个体的外显子12可变重复区域内鉴定出一个单碱基对插入,该插入导致212个氨基酸的移码,其中包括22个半胱氨酸残基,随后是一个过早的终止密码子。这是首次鉴定出导致人类疾病的AGC1突变。这一发现扩展了可能导致SED的突变基因谱,因此将有助于对这一复杂疾病组进行分子界定。