Finkelstein J E, Doege K, Yamada Y, Pyeritz R E, Graham J M, Moeschler J B, Pauli R M, Hecht J T, Francomano C A
Department of Pediatrics, Johns Hopkins University, Baltimore, MD.
Am J Hum Genet. 1991 Jan;48(1):97-102.
Achondroplasia and pseudoachondroplasia are autosomal dominant skeletal dysplasias resulting in short-limbed dwarfism. Histologic and ultrastructural studies of the cartilage in pseudoachondroplasia and in homozygous achondroplasia have suggested a structural abnormality in chondroitin sulfate proteoglycan (CSPG), a major structural protein in the extra-cellular matrix. The gene encoding CSPG core protein (CSPGCP) is thus a logical "candidate gene" for analysis in these conditions. cDNA probes encoding CSPGCP were used to identify restriction fragment length polymorphisms (RFLPs) in DNA from a panel of control individuals. No gross alterations at the CSPGCP locus were noted in DNA from 37 individuals with achondroplasia and 5 individuals with pseudoachondroplasia. In addition, allelic frequencies of the RFLPs were not significantly different among controls and patients with either condition. In one three-generation family with achondroplasia, close linkage of the CSPGCP locus and the skeletal dysplasia was excluded using a Bgl II polymorphism. Similarly, in a three-generation family with pseudoachondroplasia, the CSPGCP gene was not tightly linked to the disease phenotype. These results indicate that mutations at the chondroitin sulfate proteoglycan core protein locus do not cause achondroplasia or pseudoachondroplasia in these families.
软骨发育不全和假性软骨发育不全是常染色体显性遗传的骨骼发育不良,可导致短肢侏儒症。对假性软骨发育不全和纯合子软骨发育不全患者软骨的组织学和超微结构研究表明,硫酸软骨素蛋白聚糖(CSPG,细胞外基质中的一种主要结构蛋白)存在结构异常。因此,编码CSPG核心蛋白(CSPGCP)的基因是分析这些病症时合理的“候选基因”。使用编码CSPGCP的cDNA探针来鉴定一组对照个体DNA中的限制性片段长度多态性(RFLP)。在37名软骨发育不全患者和5名假性软骨发育不全患者的DNA中,未发现CSPGCP基因座有明显改变。此外,RFLP的等位基因频率在对照组与患有这两种病症之一的患者之间无显著差异。在一个三代均患软骨发育不全的家族中,利用Bgl II多态性排除了CSPGCP基因座与骨骼发育不良的紧密连锁关系。同样,在一个三代均患假性软骨发育不全的家族中,CSPGCP基因与疾病表型也没有紧密连锁。这些结果表明,在这些家族中,硫酸软骨素蛋白聚糖核心蛋白基因座的突变不会导致软骨发育不全或假性软骨发育不全。