Greenwood Genetic Center, 106 Gregor Mendel Circle, Greenwood, SC 29646, USA.
Mol Genet Metab. 2010 May;100(1):51-6. doi: 10.1016/j.ymgme.2010.01.004. Epub 2010 Jan 15.
Sanfilippo syndrome type B (mucopolysaccharidosis IIIB) is an autosomal recessive disease that is caused by a deficiency of the lysosomal enzyme alpha-N-acetylglucosaminidase (NAGLU). Over 100 different mutations in the NAGLU gene have been identified in Sanfilippo syndrome type B patients; however, no large deletions have been reported. Here we present the first case of a large homozygous intragenic NAGLU gene deletion identified in an affected child of consanguineous parents. Long range and multiplex PCR methods were used to characterize this deletion which encompasses exons 3 and 4 and is 1146 base pairs long. We propose that Alu element-mediated unequal homologous recombination between an Alu-Y in intron 2 and an Alu-Sx in intron 4 is the likely mechanism for this deletion, thereby contributing further insight into the molecular etiology of this disorder and providing additional evidence of its allelic heterogeneity.
黏多糖贮积症 IIIB 型(Sanfilippo 综合征 B 型)是一种常染色体隐性疾病,由溶酶体酶α-N-乙酰氨基葡萄糖苷酶(NAGLU)缺乏引起。在黏多糖贮积症 IIIB 型患者中已经发现了超过 100 种 NAGLU 基因突变;然而,尚未报道过大片段缺失。在此,我们报告了首例在受影响的近亲父母的孩子中发现的大型纯合子 NAGLU 基因内缺失的病例。使用长距离和多重 PCR 方法来鉴定该缺失,该缺失包含外显子 3 和 4,长 1146 个碱基对。我们提出,Alu 元件介导的 2 号内含子中的 Alu-Y 和 4 号内含子中的 Alu-Sx 之间的非同源性重组是这种缺失的可能机制,从而进一步深入了解该疾病的分子病因,并提供其等位基因异质性的更多证据。