Sasaki T, Tonoki H, Soejima H, Niikawa N
Department of Human Genetics, Nagasaki University School of Medicine, Japan.
J Med Genet. 1997 Apr;34(4):335-9. doi: 10.1136/jmg.34.4.335.
We report on an 11 year old girl with trichorhinophalangeal syndrome type I (TRPS1), postaxial polydactyly of the fingers, and a de novo paracentric inversion on the long arm of chromosome 8 involving bands q13.1 and q24.11. Molecular analysis using FISH and polymorphic DNA markers detected an approximately 4 Mb, cytogenetically unidentified deletion occurring between two STSs markers, AFMB331YA9 and D8S1200, around the region of the distal inversion breakpoint. Although the deletion is large, mental retardation was not present in the patient. This is the first report of a cryptic deletion in a TRPS1 patient, both ends of which were analysed at the molecular level. The data obtained are useful for defining the location of the putative mental retardation gene(s) in TRPS1 and Langer-Giedion syndrome (TRPS2), as well as a locus for postaxial polydactyly.
我们报告了一名11岁患有I型毛发鼻指综合征(TRPS1)、手指轴后多指畸形且8号染色体长臂发生涉及q13.1和q24.11带的新发臂内倒位的女孩。使用荧光原位杂交(FISH)和多态性DNA标记进行的分子分析检测到,在远端倒位断点区域周围的两个STS标记AFMB331YA9和D8S1200之间发生了一个约4 Mb的、细胞遗传学上未鉴定的缺失。尽管该缺失较大,但患者并未出现智力迟钝。这是关于TRPS1患者中隐匿性缺失的首次报告,其两端均在分子水平进行了分析。所获得的数据对于确定TRPS1和朗格-吉迪恩综合征(TRPS2)中假定的智力迟钝基因的位置以及轴后多指畸形的一个位点很有用。