Buiting K, Saitoh S, Gross S, Dittrich B, Schwartz S, Nicholls R D, Horsthemke B
Institut für Humangenetik, Universitätsklinikum Essen, Germany.
Nat Genet. 1995 Apr;9(4):395-400. doi: 10.1038/ng0495-395.
A subset of patients with Angelman and Prader-Willi syndrome have apparently normal chromosomes of biparental origin, but abnormal DNA methylation at several loci within chromosome 15q11-13, and probably have a defect in imprinting. Using probes from a newly established 160-kb contig including D15S63 (PW71) and SNRPN, we have identified inherited microdeletions in two AS families and three PWS families. The deletions probably affect a single genetic element that we term the 15q11-13 imprinting centre (IC). In our model, the IC regulates the chromatin structure, DNA methylation and gene expression in cis throughout 15q11-13. Mutations of the imprinting centre can be transmitted silently through the germline of one sex, but appear to block the resetting of the imprint in the germline of the opposite sex.
一小部分患有安吉尔曼综合征和普拉德-威利综合征的患者,其染色体显然源自双亲且看似正常,但在15号染色体长臂11-13区域的几个位点存在异常的DNA甲基化,可能存在印记缺陷。利用来自一个新建立的包含D15S63(PW71)和SNRPN的160kb重叠群的探针,我们在两个安吉尔曼综合征家系和三个普拉德-威利综合征家系中鉴定出了遗传性微缺失。这些缺失可能影响了一个单一的遗传元件,我们将其称为15号染色体长臂11-13印记中心(IC)。在我们的模型中,印记中心在顺式作用下调节整个15号染色体长臂11-13区域的染色质结构、DNA甲基化和基因表达。印记中心的突变可以通过一种性别的生殖细胞悄然传递,但似乎会阻止在异性生殖细胞中印记的重置。