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源于父源新生易位、1型邻接分离和22号染色体母源异二体的der(22)t(11;22)。

Der(22)t(11;22) resulting from a paternal de novo translocation, adjacent 1 segregation, and maternal heterodisomy of chromosome 22.

作者信息

Dawson A J, Mears A J, Chudley A E, Bech-Hansen T, McDermid H

机构信息

Department of Paediatrics and Child Health, University of Manitoba, Winnipeg, Canada.

出版信息

J Med Genet. 1996 Nov;33(11):952-6. doi: 10.1136/jmg.33.11.952.

Abstract

The t(11;22) (q23;q11) translocation is the most frequently identified familial reciprocal translocation in humans. In translocation carriers, 3:1 meiotic segregation with tertiary trisomy can occur resulting in abnormal progeny with the der(22) as the supernumary chromosome. Affected children have a distinct phenotype with multiple anomalies and severe mental retardation. We have identified a child with developmental delay and multiple anomalies consistent with the der(22) phenotype. Cytogenetic analysis showed an abnormal chromosome complement of 47,XX,+der(22)t(11;22)(q23; q11) in all 50 cells analysed. FISH analysis using chromosome 11 and 22 painting probes showed a pattern consistent with a reciprocal translocation of the distal bands 11q23 and 22q11 respectively. Parental karyotypes were normal. RFLP analysis of locus D22S43, which maps above the t(11;22) breakpoint, showed that the der(22) was paternal in origin and indicated that the normal chromosomes 22 were the probable result of maternal heterodisomy. RFLP analysis of locus D22S94, which maps below the t(11;22) breakpoint, also suggested that both normal chromosomes 22 of the child represented the two maternal homologues. Non-paternity was excluded through the analysis of 10 microsatellite markers distributed on 10 different chromosomes and three VNTRs on three different chromosomes. To the best of our knowledge, this is the first reported case of a patient with an abnormal karyotype resulting from a de novo translocation in the paternal germline with probable unbalanced adjacent 1 segregation and maternal non-disjunction of chromosome 22 in meiosis I.

摘要

t(11;22)(q23;q11)易位是人类中最常被识别出的家族性相互易位。在易位携带者中,减数分裂时会出现3:1的分离并伴有三级三体,从而产生以der(22)为额外染色体的异常后代。受影响的儿童具有独特的表型,伴有多种异常和严重智力迟钝。我们鉴定出一名发育迟缓且伴有多种异常的儿童,其表现与der(22)表型相符。细胞遗传学分析显示,在所有分析的50个细胞中,染色体组成为47,XX,+der(22)t(11;22)(q23;q11)异常。使用11号和22号染色体涂染探针的荧光原位杂交(FISH)分析显示,其模式分别与11q23和22q11远端带的相互易位一致。父母的核型正常。对位于t(11;22)断点上方的D22S43位点进行的限制性片段长度多态性(RFLP)分析表明,der(22)源自父亲,这表明正常的22号染色体可能是母亲异源二体的结果。对位于t(11;22)断点下方的D22S94位点进行的RFLP分析也表明,该儿童的两条正常22号染色体代表两条母亲同源染色体。通过对分布在10条不同染色体上的10个微卫星标记以及3条不同染色体上的3个可变数目串联重复序列(VNTR)进行分析,排除了非父系遗传的可能性。据我们所知,这是首例报道的因父系生殖系新生易位导致核型异常的病例,可能存在不平衡的相邻1分离以及减数分裂I期母亲22号染色体的不分离。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7641/1050791/c139d44897c7/jmedgene00265-0065-a.jpg

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