Frosk Patrick, Weiler Tracey, Nylen Edward, Sudha Thangirala, Greenberg Cheryl R, Morgan Kenneth, Fujiwara T Mary, Wrogemann Klaus
Departments of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Manitoba, Canada.
Am J Hum Genet. 2002 Mar;70(3):663-72. doi: 10.1086/339083. Epub 2002 Jan 29.
Limb-girdle muscular dystrophy type 2H (LGMD2H) is a mild autosomal recessive myopathy that was first described in the Manitoba Hutterite population. Previous studies in our laboratory mapped the causative gene for this disease to a 6.5-Mb region in chromosomal region 9q31-33, flanked by D9S302 and D9S1850. We have now used additional families and a panel of 26 microsatellite markers to construct haplotypes. Twelve recombination events that reduced the size of the candidate region to 560 kb were identified or inferred. This region is flanked by D9S1126 and D9S737 and contains at least four genes. Exons of these genes were sequenced in one affected individual, and four sequence variations were identified. The families included in our study and 100 control individuals were tested for these variations. On the basis of our results, the mutation in the tripartite-motif-containing gene (TRIM32) that replaces aspartate with asparagine at position 487 appears to be the causative mutation of LGMD2H. All affected individuals were found to be homozygous for D487N, and this mutation was not found in any of the controls. This mutation occurs in an NHL (named after the proteins NCL1, HT2A, and LIN-41) domain at a position that is highly conserved. NHL domains are known to be involved in protein-protein interactions. Although the function of TRIM32 is unknown, current knowledge of the domain structure of this protein suggests that it may be an E3-ubiquitin ligase. If proven, this represents a new pathogenic mechanism leading to muscular dystrophy.
2H型肢带型肌营养不良症(LGMD2H)是一种轻度常染色体隐性肌病,最初在曼尼托巴胡特尔人群中被描述。我们实验室之前的研究将该疾病的致病基因定位到染色体9q31 - 33区域的一个6.5兆碱基区域,两侧分别是D9S302和D9S1850。我们现在利用更多的家系和一组26个微卫星标记构建单倍型。识别或推断出12个重组事件,这些事件将候选区域缩小到560千碱基。该区域两侧是D9S1126和D9S737,包含至少四个基因。在一名受影响个体中对这些基因的外显子进行了测序,鉴定出四个序列变异。对我们研究中纳入的家系和100名对照个体进行了这些变异的检测。根据我们的结果,含三联基序的基因(TRIM32)中第487位天冬氨酸被天冬酰胺取代的突变似乎是LGMD2H的致病突变。所有受影响个体均被发现为D487N纯合子,而在任何对照个体中均未发现该突变。此突变发生在一个高度保守位置的NHL(以蛋白质NCL1、HT2A和LIN - 41命名)结构域。已知NHL结构域参与蛋白质 - 蛋白质相互作用。尽管TRIM32的功能尚不清楚,但目前对该蛋白质结构域结构的了解表明它可能是一种E3泛素连接酶。如果得到证实,这代表了一种导致肌营养不良症的新致病机制。