Funke B, Edelmann L, McCain N, Pandita R K, Ferreira J, Merscher S, Zohouri M, Cannizzaro L, Shanske A, Morrow B E
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Am J Hum Genet. 1999 Mar;64(3):747-58. doi: 10.1086/302284.
Derivative 22 (der[22]) syndrome is a rare disorder associated with multiple congenital anomalies, including profound mental retardation, preauricular skin tags or pits, and conotruncal heart defects. It can occur in offspring of carriers of the constitutional t(11;22)(q23;q11) translocation, owing to a 3:1 meiotic malsegregation event resulting in partial trisomy of chromosomes 11 and 22. The trisomic region on chromosome 22 overlaps the region hemizygously deleted in another congenital anomaly disorder, velo-cardio-facial syndrome/DiGeorge syndrome (VCFS/DGS). Most patients with VCFS/DGS have a similar 3-Mb deletion, whereas some have a nested distal deletion endpoint resulting in a 1.5-Mb deletion, and a few rare patients have unique deletions. To define the interval on 22q11 containing the t(11;22) breakpoint, haplotype analysis and FISH mapping were performed for five patients with der(22) syndrome. Analysis of all the patients was consistent with 3:1 meiotic malsegregation in the t(11;22) carrier parent. FISH-mapping studies showed that the t(11;22) breakpoint occurred in the same interval as the 1.5-Mb distal deletion breakpoint for VCFS. The deletion breakpoint of one VCFS patient with an unbalanced t(18;22) translocation also occurred in the same region. Hamster-human somatic hybrid cell lines from a patient with der(22) syndrome and a patient with VCFS showed that the breakpoints occurred in an interval containing low-copy repeats, distal to RANBP1 and proximal to ZNF74. The presence of low-copy repetitive sequences may confer susceptibility to chromosome rearrangements. A 1.5-Mb region of overlap on 22q11 in both syndromes suggests the presence of dosage-dependent genes in this interval.
衍生 22(der[22])综合征是一种罕见的疾病,与多种先天性异常相关,包括严重智力发育迟缓、耳前皮肤赘生物或凹痕以及圆锥动脉干心脏缺陷。它可发生于携带染色体结构畸变 t(11;22)(q23;q11)的亲代的后代中,这是由于减数分裂过程中 3:1 的错误分离事件导致 11 号和 22 号染色体部分三体化。22 号染色体上的三体区域与另一种先天性异常疾病——腭心面综合征/迪格奥尔格综合征(VCFS/DGS)中半合子缺失的区域重叠。大多数 VCFS/DGS 患者有类似的 3Mb 缺失,而一些患者有嵌套的远端缺失端点,导致 1.5Mb 缺失,少数罕见患者有独特的缺失。为了确定 22q11 上包含 t(11;22)断点的区间,对 5 例 der(22)综合征患者进行了单倍型分析和荧光原位杂交(FISH)定位。对所有患者的分析均与 t(11;22)携带者亲代中 3:1 的减数分裂错误分离一致。FISH 定位研究表明,t(11;22)断点与 VCFS 的 1.5Mb 远端缺失断点位于同一区间。一名患有不平衡 t(18;22)易位的 VCFS 患者的缺失断点也发生在同一区域。来自一名 der(22)综合征患者和一名 VCFS 患者的仓鼠 - 人类体细胞杂交细胞系表明,断点发生在一个包含低拷贝重复序列的区间内,该区间位于 RANBP1 远端且 ZNF74 近端。低拷贝重复序列的存在可能会使染色体重排更易发生。两种综合征在 22q11 上有 1.5Mb 的重叠区域,提示该区间存在剂量依赖性基因。