Férec Claude, Casals Teresa, Chuzhanova Nadia, Macek Milan, Bienvenu Thierry, Holubova Andrea, King Caitriona, McDevitt Trudi, Castellani Carlo, Farrell Philip M, Sheridan Molly, Pantaleo Sarah-Jane, Loumi Ourida, Messaoud Taieb, Cuppens Harry, Torricelli Francesca, Cutting Garry R, Williamson Robert, Ramos Maria Jesus Alonso, Pignatti Pier Franco, Raguénès Odile, Cooper David N, Audrézet Marie-Pierre, Chen Jian-Min
INSERM, U613 (Génétique Moléculaire et Génétique Epidémiologique), Brest, France.
Eur J Hum Genet. 2006 May;14(5):567-76. doi: 10.1038/sj.ejhg.5201590.
Gross genomic rearrangements involving deletions in the CFTR gene have recently been found to account for approximately 20% of unidentified cystic fibrosis (CF) chromosomes in both French and Italian patients. Using QMPSF and walking quantitative DHPLC, six novel mutations (three simple deletions, two complex deletions with short insertions of 3-6 bp, and a complex deletion with a 182 bp inverted downstream sequence) were characterized by screening 274 unidentified CF chromosomes from 10 different countries. These lesions increase the total number of fully characterized large CFTR genomic rearrangements involving deletions to 21. Systematic analysis of the 42 associated breakpoints indicated that all 21 events were caused by nonhomologous recombination. Whole gene complexity analysis revealed a significant correlation between regions of low sequence complexity and the locations of the deletion breakpoints. Known recombination-promoting motifs were noted in the vicinity of the breakpoints. A total of 11 simple deletions were potentially explicable in terms of the classical model of replication slippage. However, the complex deletions appear to have arisen via multiple mechanisms; three of the five complex deletions with short insertions and both examples of large inverted insertions (299 and 182 bp, respectively) can be explained by either a model of serial replication slippage in cis (SRScis) or SRS in trans (SRStrans). Finally, the nature and distribution of large genomic rearrangements in the CFTR gene were compared and contrasted with those of two other genes, DMD and MSH2, with a view to gaining a broader understanding of DNA sequence context in mediating the diverse underlying mutational mechanisms.
最近发现,涉及囊性纤维化跨膜传导调节因子(CFTR)基因缺失的基因组重排大约占法国和意大利患者中未明确的囊性纤维化(CF)染色体的20%。通过使用QMPSF和步移定量变性高效液相色谱法(DHPLC),对来自10个不同国家的274条未明确的CF染色体进行筛查,鉴定出6个新突变(3个简单缺失、2个带有3 - 6 bp短插入的复杂缺失以及1个带有182 bp下游反向序列的复杂缺失)。这些病变使已完全鉴定的涉及缺失的CFTR基因组大重排总数增加到21个。对42个相关断点的系统分析表明,所有21个事件均由非同源重组引起。全基因复杂性分析显示,低序列复杂性区域与缺失断点位置之间存在显著相关性。在断点附近发现了已知的促进重组的基序。共有11个简单缺失根据经典的复制滑移模型可能是可以解释的。然而,复杂缺失似乎是通过多种机制产生的;5个带有短插入的复杂缺失中的3个以及两个大的反向插入实例(分别为299和182 bp)可以通过顺式串联复制滑移模型(SRScis)或反式串联复制滑移模型(SRStrans)来解释。最后,将CFTR基因中大基因组重排的性质和分布与另外两个基因——杜氏肌营养不良症(DMD)基因和错配修复蛋白2(MSH2)基因进行了比较和对比,以期更广泛地了解DNA序列背景在介导各种潜在突变机制中的作用。