Marian A J, Yu Q T, Mares A, Hill R, Roberts R, Perryman M B
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.
J Clin Invest. 1992 Dec;90(6):2156-65. doi: 10.1172/JCI116101.
Familial hypertrophic cardiomyopathy (FHCM) is an autosomal dominant disease affecting primarily the myocardium. The gene responsible for FHCM has been localized to chromosome 14 in some families and several mutations have been described in the beta-myosin heavy chain (beta MHC), a candidate gene for the disease. We recently identified a family with HCM in whom we did not detect any of the known mutations in the beta MHC gene (the alpha/beta MHC hybrid gene and the missense mutation in exons 13 and 9). However, we did observe a novel 9.5-kb BamHI restriction fragment length polymorphism detected by a beta MHC probe on Southern blots of DNA from the proband of this family. Similarly, a novel 3.8-kb TaqI polymorphism and a novel 4.3-kb HindIII polymorphism were detected on Southern blots of DNA from the same proband. Polymerase chain reaction (PCR) was used to amplify the segment of the beta MHC that was detected by pSC14 probe. PCR amplification of the distal 3'-end of the beta MHC gene yielded an additional product in the DNA template from the proband which was subsequently cloned and sequenced. The sequence analysis showed a 2.4-kb nucleotide deletion involving one allele of the beta MHC gene. The deletion includes part of the intron 39, exon 40 including the 3'-untranslated region and the polyadenylation signal, and part of the beta-alpha MHC intergenic region. This deletion was inherited in Mendelian fashion in an additional three members of this small family of which only the proband has developed clinically diagnosed HCM at a very late onset (age 59 yr), the other three family members are younger and have not developed the disease at the ages of 10, 32, and 33 yr.
家族性肥厚型心肌病(FHCM)是一种主要影响心肌的常染色体显性疾病。在一些家族中,导致FHCM的基因已定位到14号染色体,并且在β-肌球蛋白重链(βMHC)中描述了几种突变,βMHC是该疾病的一个候选基因。我们最近鉴定了一个患有肥厚型心肌病(HCM)的家族,在该家族中我们未检测到βMHC基因中的任何已知突变(α/βMHC杂交基因以及外显子13和9中的错义突变)。然而,我们确实观察到通过βMHC探针在该家族先证者的DNA Southern印迹上检测到一种新的9.5kb BamHI限制性片段长度多态性。同样,在来自同一位先证者的DNA Southern印迹上检测到一种新的3.8kb TaqI多态性和一种新的4.3kb HindIII多态性。聚合酶链反应(PCR)用于扩增由pSC14探针检测到的βMHC片段。βMHC基因远端3'端的PCR扩增在来自先证者的DNA模板中产生了一个额外的产物,随后对其进行克隆和测序。序列分析显示βMHC基因的一个等位基因存在2.4kb的核苷酸缺失。该缺失包括内含子39的一部分、外显子40(包括3'非翻译区和聚腺苷酸化信号)以及β-αMHC基因间区域的一部分。这种缺失以孟德尔方式在这个小家族的另外三名成员中遗传,其中只有先证者在很晚的发病年龄(59岁)出现了临床诊断的HCM,其他三名家族成员较年轻,在10岁、32岁和33岁时未患该疾病。