Holm I A, Huang X, Kunkel L M
Division of Genetics, Children's Hospital, Boston, MA 02115, USA.
Am J Hum Genet. 1997 Apr;60(4):790-7.
X-linked hypophosphatemic rickets (HYP) is a dominant disorder characterized by renal phosphate wasting and abnormal vitamin D metabolism. PEX, the gene that is defective in HYP and is located on Xp22.1, is homologous to members of the neutral endopeptidase family. However, the complete coding sequence of the PEX cDNA, the structure of the PEX gene, and the role that PEX plays in phosphate transport remain unknown. We determined the genomic structure of the published PEX gene, which was found to be composed of 18 short exons, and demonstrated that the genomic organization of PEX shares homology to members of the family of neutral endopeptidases. Primer sets were designed from the intron sequence, to amplify each PEX exon from genomic DNA of HYP patients. Mutations in PEX were identified in 9/22 unrelated HYP patients, confirming that defects in PEX are responsible for HYP. The mutations detected included three nonsense mutations, a 1-bp deletion leading to a frameshift, a donor splice-site mutation, and missense mutations in four patients. Although the entire PEX gene has not been identified and some mutations may have been missed, the lack of detection of mutations in the remaining 13 patients, especially in 1 patient who has an apparently balanced, de novo 9;13 translocation, implies that there may be other loci involved in the generation of the HYP phenotype.
X连锁低磷性佝偻病(HYP)是一种显性疾病,其特征为肾性磷酸盐流失和维生素D代谢异常。PEX基因位于Xp22.1,是导致HYP的缺陷基因,与中性内肽酶家族成员同源。然而,PEX cDNA的完整编码序列、PEX基因的结构以及PEX在磷酸盐转运中的作用仍不清楚。我们确定了已发表的PEX基因的基因组结构,发现它由18个短外显子组成,并证明PEX的基因组组织与中性内肽酶家族成员具有同源性。根据内含子序列设计引物对,以从HYP患者的基因组DNA中扩增每个PEX外显子。在22名无亲缘关系的HYP患者中,有9名患者检测到PEX基因突变,证实PEX缺陷是导致HYP的原因。检测到的突变包括三个无义突变、一个导致移码的1个碱基缺失、一个供体剪接位点突变以及四名患者中的错义突变。尽管尚未鉴定出整个PEX基因,可能遗漏了一些突变,但在其余13名患者中未检测到突变,尤其是在一名具有明显平衡的新发9;13易位的患者中未检测到突变,这意味着可能还有其他基因座参与了HYP表型的产生。