Bargal Ruth, Zeigler Marsha, Abu-Libdeh Bassam, Zuri Vivi, Mandel Hanna, Ben Neriah Ziva, Stewart Fiona, Elcioglu Nursel, Hindi Tareq, Le Merrer Martine, Bach Gideon, Raas-Rothschild Annick
Department of Human Genetics, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Mol Genet Metab. 2006 Aug;88(4):359-63. doi: 10.1016/j.ymgme.2006.03.003. Epub 2006 Apr 21.
Mucolipidosis II (ML II) and Mucolipidosis type III (ML III) are autosomal recessive disorders of lysosomal hydrolases trafficking due to the deficiency of the multimeric enzyme, UDP-N-acetylglucosamine-1-phosphotransferase. The alpha/beta subunits encoded by the GNPTA gene is the catalytic subunit of the enzyme while the gamma recognition subunit is encoded by the GNPTAG gene. We report the molecular analysis of GNPTA in 21 families with ML II and 3 families with ML III. The ML II mutant genotypes included three splice-site mutations [IVS1-2A>G; IVS17+1G>A; IVS18+1G>A] in seven Palestinian, Israeli Arab-Muslims, and Turkish patients; a two base pair deletion [c.3503_4delTC] [corrected] in 11 patients from Israel, Turkey, and Ireland; two nonsense mutations [c.2533C>T (Q845X); c.3613C>T (R1205X)], in a Turkish and an Arab-Muslim patient from the Nablus area, respectively, and an insertion mutation [c.2916insT] in a patient from Nablus. The ML III mutant genotypes included a splice-site mutation [IVS17+6T>G] in two patients from Irish/Scottish origin who were compound heterozygous for a nonsense mutation [c.3565C>T (R1189X)] and the deletion mutation [c.3503_4delTC] [corrected] respectively. The third ML III patient from France was compound heterozygous for a missense mutation [c.1196C>T] and the same deletion [c.3503_4delTC] [corrected] found homozygous in 11 ML II patients. The 21 ML II patients were homozygous while the three ML III patients were compound heterozygous for mutations in GNPTA. The results of this study confirm that ML II or ML III phenotype is not due to the localization of the mutations, but rather to the severity of the mutations, ML II and ML III might be allelic, and ML III is genetically heterogeneous. We suggest that the diseases due to mutations in GNPTA represent a clinical continuum between ML III and ML II, and the classification of these diseases should be based on the age of onset, clinical symptoms, and severity.
粘脂贮积症II型(ML II)和粘脂贮积症III型(ML III)是溶酶体水解酶运输的常染色体隐性疾病,病因是多聚体酶UDP-N-乙酰葡糖胺-1-磷酸转移酶缺乏。由GNPTA基因编码的α/β亚基是该酶的催化亚基,而γ识别亚基由GNPTAG基因编码。我们报告了对21个ML II家庭和3个ML III家庭的GNPTA分子分析。ML II突变基因型包括7名巴勒斯坦、以色列阿拉伯穆斯林和土耳其患者中的3个剪接位点突变[IVS1-2A>G;IVS17+1G>A;IVS18+1G>A];11名来自以色列、土耳其和爱尔兰患者中的一个两碱基对缺失[c.3503_4delTC] [校正后];分别在一名土耳其患者和一名来自纳布卢斯地区的阿拉伯穆斯林患者中的2个无义突变[c.2533C>T (Q845X);c.3613C>T (R1205X)],以及一名来自纳布卢斯患者中的一个插入突变[c.2916insT]。ML III突变基因型包括2名爱尔兰/苏格兰裔患者中的一个剪接位点突变[IVS17+6T>G],他们分别是无义突变[c.3565C>T (R1189X)]和缺失突变[c.3503_4delTC] [校正后]的复合杂合子。第三名来自法国的ML III患者是错义突变[c.1196C>T]和在11名ML II患者中发现的相同缺失[c.3503_4delTC] [校正后]的复合杂合子。21名ML II患者是纯合子,而3名ML III患者是GNPTA突变的复合杂合子。本研究结果证实,ML II或ML III表型并非由突变的定位所致,而是由突变的严重程度决定,ML II和ML III可能是等位基因,且ML III在遗传上具有异质性。我们认为,由GNPTA突变引起的疾病代表了ML III和ML II之间的临床连续体, 这些疾病的分类应基于发病年龄、临床症状和严重程度。