Moloney D M, Slaney S F, Oldridge M, Wall S A, Sahlin P, Stenman G, Wilkie A O
Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, UK.
Nat Genet. 1996 May;13(1):48-53. doi: 10.1038/ng0596-48.
Apert syndrome results from one or other of two specific nucleotide substitutions, both C-->G transversions, in the fibroblast growth factor receptor 2 (FGFR2) gene. The frequency of new mutations, estimated as 1 per 65,000 live births, implies germline transversion rates at these two positions are currently the highest known in the human genome. Using a novel application of the amplification refractory mutation system (ARMS), we have determined the parental origin of the new mutation in 57 Apert families: in every case, the mutation arose from the father. This identifies the biological basis of the paternal age effect for new mutations previously suggested for this disorder.
Apert综合征是由成纤维细胞生长因子受体2(FGFR2)基因中两种特定的核苷酸取代之一引起的,这两种取代均为C→G颠换。新突变的频率估计为每65000例活产中有1例,这意味着这两个位置的种系颠换率是目前人类基因组中已知最高的。通过对扩增阻滞突变系统(ARMS)的一种新应用,我们确定了57个Apert家族中新突变的亲本来源:在每种情况下,突变均来自父亲。这确定了先前针对该疾病所提出的新突变的父龄效应的生物学基础。