Smith Frances J D, Morley Susan M, McLean W H Irwin
Epithelial Genetics Group, Human Genetics Unit, Ninewells Medical School, University of Dundee, UK.
J Invest Dermatol. 2004 Jan;122(1):73-7. doi: 10.1046/j.0022-202X.2003.22129.x.
The severe Dowling-Meara form of epidermolysis bullosa simplex is caused by dominant-negative mutations in keratins 5 and 14, which are specifically expressed in the basal keratinocytes of the epidermis. The most common mutation in the Dowling-Meara form of epidermolysis bullosa simplex patients is the missense mutation R125C in exon 1 of the K14 gene. We made a primary keratinocyte cell line from a sporadic case known to carry the R125C mutation as part of an ongoing gene therapy initiative. The full-length K14 cDNA was sequenced using keratinocyte mRNA. Unexpectedly, a second mutation was identified in K14: a heterozygous 1 bp insertion mutation (242insG) upstream of the R125C mutation. This frameshift mutation creates a premature termination codon immediately downstream, thereby nullifying the dominant-negative allele. The second mutation was only present in DNA derived from keratinocytes and was absent from lymphocyte DNA. This case represents a novel mechanism of revertant mosaicism and is an example of "natural gene therapy".
单纯性大疱性表皮松解症的严重Dowling-Meara型是由角蛋白5和14的显性负性突变引起的,这两种角蛋白在表皮的基底角质形成细胞中特异性表达。单纯性大疱性表皮松解症Dowling-Meara型患者最常见的突变是K14基因第1外显子中的错义突变R125C。作为正在进行的基因治疗计划的一部分,我们从一个已知携带R125C突变的散发病例中建立了一个原代表皮角质形成细胞系。使用角质形成细胞mRNA对全长K14 cDNA进行测序。出乎意料的是,在K14中发现了第二个突变:在R125C突变上游的一个杂合的1 bp插入突变(242insG)。这种移码突变在紧接下游产生一个提前终止密码子,从而使显性负性等位基因无效。第二个突变仅存在于源自角质形成细胞的DNA中,而在淋巴细胞DNA中不存在。该病例代表了一种回复性镶嵌现象的新机制,是“自然基因治疗”的一个例子。