Hunter A G, Jacob P, O'Hoy K, MacDonald I, Mettler G, Tsilfidis C, Korneluk R G
Department of Genetics, Children's Hospital of Eastern Ontario, Ottawa, Canada.
Am J Med Genet. 1993 Feb 1;45(3):401-7. doi: 10.1002/ajmg.1320450330.
Recently an unstable trinucleotide CTG repeat, located within the 3' untranslated region of a gene on 19q13.3 was discovered in kindreds with myotonic dystrophy (DM). The age-of-onset/severity of DM shows a good correlation with CTG repeat size, and pedigrees and data reported to date have shown a striking trend toward amplification of the size of the CTG repeat during transmission from parent to child. The amplification has been accepted as the biological explanation for anticipation in the clinical severity observed in many families with DM. In this paper we report on 3 families where CTG amplification decreased during transmission from parent to child. In one case there was a gene conversion event, while in the remaining 2 there was a simpler reduction in the size of the repeat length. The changes appear to have been accompanied by a reduction in clinical severity in the child when compared to the parent. These observations are discussed in terms of their clinical implications and the biases that may exist in much of the reported data.
最近,在患有强直性肌营养不良(DM)的家族中发现了一个不稳定的三核苷酸CTG重复序列,它位于19q13.3上一个基因的3'非翻译区。DM的发病年龄/严重程度与CTG重复序列的大小呈现出良好的相关性,并且迄今为止报道的家系和数据显示,在从父母向子女传递的过程中,CTG重复序列的大小有显著的扩增趋势。这种扩增已被公认为是许多DM家族中临床严重程度出现遗传早现现象的生物学解释。在本文中,我们报告了3个家族,其中CTG扩增在从父母向子女传递的过程中减少。在一个案例中发生了基因转换事件,而在其余2个案例中,重复长度的大小有更简单的减少。与父母相比,这些变化似乎伴随着子女临床严重程度的降低。我们从这些观察结果的临床意义以及许多已报道数据中可能存在的偏差方面进行了讨论。