Pasmant Eric, de Saint-Trivier Aurélie, Laurendeau Ingrid, Dieux-Coeslier Anne, Parfait Béatrice, Vidaud Michel, Vidaud Dominique, Bièche Ivan
UMR745 INSERM, Université Paris Descartes, Faculté des Sciences Pharmaceutiques et Biologiques, Paris, France.
Eur J Hum Genet. 2008 Dec;16(12):1459-66. doi: 10.1038/ejhg.2008.134. Epub 2008 Jul 23.
We describe a large germline deletion removing the NF1 locus, identified by heterozygosity mapping based on microsatellite markers, in an 8-year-old French girl with a particularly severe NF1 contiguous gene syndrome. We used gene-dose mapping with sequence-tagged site real-time PCR to locate the deletion end points, which were precisely characterized by means of long-range PCR and nucleotide sequencing. The deletion is located on chromosome arm 17q and is exactly 7 586 986 bp long. It encompasses the entire NF1 locus and about 100 other genes, including numerous chemokine genes, an attractive in silico-selected cerebrally expressed candidate gene (designated NUFIP2, for nuclear fragile X mental retardation protein interacting protein 2; NM_020772) and four microRNA genes. Interestingly, the centromeric breakpoint is located in intron 4 of the PIPOX gene (pipecolic acid oxidase; NM_016518) and the telomeric breakpoint in intron 5 of the GGNBP2 gene (gametogenetin binding protein 2; NM_024835) coding a transcription factor. As PIPOX and GGNBP2 have the same transcriptional orientation, we postulated, and then confirmed, the existence of a chimeric transcript. This transcript, and/or haploinsufficiency of one or several deleted genes, could explain the clinical severity of the syndrome in this patient.
我们描述了一个大型种系缺失,该缺失移除了NF1基因座,通过基于微卫星标记的杂合性定位在一名患有特别严重的NF1连续基因综合征的8岁法国女孩中得以确定。我们使用序列标签位点实时PCR进行基因剂量定位来确定缺失端点,通过长距离PCR和核苷酸测序对其进行了精确表征。该缺失位于17号染色体长臂上,长度恰好为7586986 bp。它涵盖了整个NF1基因座以及约100个其他基因,包括众多趋化因子基因、一个通过计算机模拟选择的、在大脑中表达的有吸引力的候选基因(命名为NUFIP2,即核脆性X智力低下蛋白相互作用蛋白2;NM_020772)和四个微小RNA基因。有趣的是,着丝粒断点位于PIPOX基因(哌啶酸氧化酶;NM_016518)的第4内含子中,端粒断点位于编码转录因子的GGNBP2基因(配子生成素结合蛋白2;NM_024835)的第5内含子中。由于PIPOX和GGNBP2具有相同的转录方向,我们推测并随后证实了嵌合转录本的存在。该转录本和/或一个或多个缺失基因的单倍剂量不足可能解释了该患者综合征的临床严重程度。