Heath K E, Campos-Barros A, Toren A, Rozenfeld-Granot G, Carlsson L E, Savige J, Denison J C, Gregory M C, White J G, Barker D F, Greinacher A, Epstein C J, Glucksman M J, Martignetti J A
Department of Human Genetics, Mount Sinai School of Medicine, New York, NY 10029, USA.
Am J Hum Genet. 2001 Nov;69(5):1033-45. doi: 10.1086/324267. Epub 2001 Oct 4.
May-Hegglin anomaly (MHA) and Fechtner (FTNS) and Sebastian (SBS) syndromes are autosomal dominant platelet disorders that share macrothrombocytopenia and characteristic leukocyte inclusions. FTNS has the additional clinical features of nephritis, deafness, and cataracts. Previously, mutations in the nonmuscle myosin heavy chain 9 gene (MYH9), which encodes nonmuscle myosin heavy chain IIA (MYHIIA), were identified in all three disorders. The spectrum of mutations and the genotype-phenotype and structure-function relationships in a large cohort of affected individuals (n=27) has now been examined. Moreover, it is demonstrated that MYH9 mutations also result in two other FTNS-like macrothrombocytopenia syndromes: Epstein syndrome (EPS) and Alport syndrome with macrothrombocytopenia (APSM). In all five disorders, MYH9 mutations were identified in 20/27 (74%) affected individuals. Four mutations, R702C, D1424N, E1841K, and R1933X, were most frequent. R702C and R702H mutations were only associated with FTNS, EPS, or APSM, thus defining a region of MYHIIA critical in the combined pathogenesis of macrothrombocytopenia, nephritis, and deafness. The E1841K, D1424N, and R1933X coiled-coil domain mutations were common to both MHA and FTNS. Haplotype analysis using three novel microsatellite markers revealed that three E1841K carriers--one with MHA and two with FTNS--shared a common haplotype around the MYH9 gene, suggesting a common ancestor. The two new globular-head mutations, K371N and R702H, as well as the recently identified MYH9 mutation, R705H, which results in DFNA17, were modeled on the basis of X-ray crystallographic data. Altogether, our data suggest that MHA, SBS, FTNS, EPS, and APSM comprise a phenotypic spectrum of disorders, all caused by MYH9 mutations. On the basis of our genetic analyses, the name "MYHIIA syndrome" is proposed to encompass all of these disorders.
May-Hegglin异常(MHA)、Fechtner综合征(FTNS)和Sebastian综合征(SBS)是常染色体显性遗传性血小板疾病,其共同特征为巨血小板减少症和特征性白细胞包涵体。FTNS还有肾炎、耳聋和白内障等额外的临床特征。此前,在这三种疾病中均发现了非肌肉肌球蛋白重链9基因(MYH9)的突变,该基因编码非肌肉肌球蛋白重链IIA(MYHIIA)。现在已经对一大群受影响个体(n = 27)中的突变谱以及基因型-表型和结构-功能关系进行了研究。此外,还证明MYH9突变还会导致另外两种类似FTNS的巨血小板减少症综合征:爱泼斯坦综合征(EPS)和伴有巨血小板减少症的Alport综合征(APSM)。在所有这五种疾病中,27名受影响个体中有20名(74%)检测到MYH9突变。四种突变,即R702C、D1424N、E1841K和R1933X最为常见。R702C和R702H突变仅与FTNS、EPS或APSM相关,因此确定了MYHIIA中一个对巨血小板减少症、肾炎和耳聋联合发病机制至关重要的区域。E1841K、D1424N和R1933X螺旋-螺旋结构域突变在MHA和FTNS中都很常见。使用三个新的微卫星标记进行单倍型分析发现,三名E1841K携带者(一名患有MHA,两名患有FTNS)在MYH9基因周围共享一个共同的单倍型,表明有共同的祖先。根据X射线晶体学数据对两个新的球状头部突变K371N和R702H以及最近发现的导致DFNA17的MYH9突变R705H进行了建模。总之,我们的数据表明,MHA、SBS、FTNS、EPS和APSM构成了一系列表型疾病,均由MYH9突变引起。基于我们的基因分析,建议使用“MYHIIA综合征”这一名称来涵盖所有这些疾病。