Groenen P M, Garcia E, Thoelen R, Aly M, Schoenmakers E F, Devriendt K, Fryns J P, Van de Ven W J
Laboratory for Molecular Oncology, Center for Human Genetics, University of Leuven(Belgium).
Cytogenet Cell Genet. 1996;75(4):210-5. doi: 10.1159/000134485.
Hydronephrosis caused by pelvi-ureteric junction obstruction (PUJO) is a frequent urological malformation assumed to result from a deficient development of the ureteric bud. The exact etiology of pelvi-ureteric junction stenosis is unknown, but there is convincing evidence for a genetic cause, with linkage analysis predicting a hereditary hydronephrosis locus on chromosome 6p. We encountered a patient with a de novo autosomal t(6;19)(p21;q13.1) and attendant bilateral multicystic renal dysplasia (MRD), bilateral PUJO resulting in massive hydronephrosis, and an associated von Mayer-Rokitansky-Kuster disorder. On the basis of the presumption that in this patient the putative hydronephrosis gene might be disrupted by the translocation, we sought to isolate DNA from the breakpoint regions as the initial step in a strategy to identify genes affected by the t(6; 19). Using sequential rounds of fluorescence in situ hybridization (FISH) with cosmids selected from a detailed integrated map of the long arm of chromosome 19, we have identified a cosmid clone that spans the breakpoint. The position of the breakpoint was further localized by Southern blot analysis. Using a vectorette PCR approach, rearranged DNA fragments were isolated and, by comparative nucleotide sequence analysis, these were shown to contain ectopic sequences. A cosmid clone containing these ectopic sequences was isolated and shown by CASH (chromosome assignment using somatic cell hybrids) and FISH (fluorescence in situ hybridization) analysis to map to the short arm of chromosome 6 and to span the breakpoint found in the MRD patient. The isolated cosmid clones are useful reagents for analysis of other MRD patients and for the search for genes at or flanking the breakpoints.
肾盂输尿管连接部梗阻(PUJO)所致肾积水是一种常见的泌尿系统畸形,被认为是由于输尿管芽发育缺陷所致。肾盂输尿管连接部狭窄的确切病因尚不清楚,但有令人信服的证据表明其与遗传因素有关,连锁分析预测6号染色体短臂上存在一个遗传性肾积水基因座。我们遇到了一名患有新发常染色体t(6;19)(p21;q13.1)以及双侧多囊性肾发育不良(MRD)、双侧PUJO导致大量肾积水和相关的 Mayer-Rokitansky-Kuster 综合征的患者。基于这样的推测,即该患者中假定的肾积水基因可能因易位而被破坏,我们试图从断点区域分离DNA,作为识别受t(6;19)影响的基因的策略的第一步。通过对从19号染色体长臂的详细整合图谱中选择的黏粒进行连续几轮荧光原位杂交(FISH),我们鉴定出了一个跨越断点的黏粒克隆。通过Southern印迹分析进一步确定了断点的位置。使用载体PCR方法,分离出重排的DNA片段,通过比较核苷酸序列分析,显示这些片段包含异位序列。分离出一个包含这些异位序列的黏粒克隆,通过体细胞杂交染色体定位(CASH)和荧光原位杂交(FISH)分析表明,该克隆定位于6号染色体短臂,并跨越MRD患者中发现的断点。分离出的黏粒克隆是分析其他MRD患者以及寻找断点处或其侧翼基因的有用试剂。