Farwell Gonzalez Kelly D, Li Xiang, Lu Hsiao-Mei, Lu Hong, Pellegrino Joan E, Miller Ryan T, Zeng Wenqi, Chao Elizabeth C
Ambry Genetics, 15 Argonaut, Aliso Viejo, CA, 92656, USA,
JIMD Rep. 2015;15:29-37. doi: 10.1007/8904_2014_294. Epub 2014 Mar 25.
Disorders of cobalamin deficiency are a heterogeneous group of disorders with at least 19 autosomal recessive-associated genes. Familial samples of an infant who died due to presumed cobalamin deficiency were referred for clinical exome sequencing. The patient died before obtaining a blood sample or skin biopsy, autopsy was declined, and DNA yielded from the newborn screening blood spot was insufficient for diagnostic testing. Whole-exome sequencing of the mother, father, and unaffected sister and tailored bioinformatics analysis was applied to search for mutations in underlying disorders with recessive inheritance. This approach identified alterations within two genes, each of which was carried by one parent. The mother carried a missense alteration in the MTR gene (c.3518C>T; p.P1173L) which was absent in the father and the sister. The father carried a translational frameshift alteration in the LMBRD1 gene (c.1056delG; p.L352Lfs*18) which was absent in the mother and present in the heterozygous state in the sister. These mutations in the MTR (MIM# 156570) and LMBRD1 (MIM# 612625) genes have been described in patients with disorders of cobalamin metabolism complementation groups cblG and cblF, respectively. The child's clinical presentation and biochemical results demonstrated overlap with both cblG and cblF. Sanger sequencing using DNA from the infant's blood spot confirmed the inheritance of the two alterations in compound heterozygous form. We present the first example of exome sequencing leading to a diagnosis in the absence of the affected patient. Furthermore, the data support the possibility for potential digenic inheritance associated with cobalamin deficiency.
钴胺素缺乏症是一组异质性疾病,至少有19个常染色体隐性相关基因。一名因疑似钴胺素缺乏症死亡的婴儿的家族样本被送去进行临床外显子组测序。该患者在采集血样或皮肤活检之前就已死亡,家属拒绝了尸检,新生儿筛查血斑提取的DNA不足以进行诊断检测。对母亲、父亲和未受影响的姐姐进行全外显子组测序,并应用定制的生物信息学分析来寻找隐性遗传的潜在疾病中的突变。这种方法在两个基因中发现了变异,每个基因由一位家长携带。母亲在MTR基因中携带一个错义变异(c.3518C>T;p.P1173L),父亲和姐姐中没有。父亲在LMBRD1基因中携带一个翻译移码变异(c.1056delG;p.L352Lfs*18),母亲中没有,姐姐中呈杂合状态。MTR(MIM# 156570)和LMBRD1(MIM# 612625)基因中的这些突变分别在钴胺素代谢互补组cblG和cblF的疾病患者中被描述过。该患儿的临床表现和生化结果显示与cblG和cblF均有重叠。使用婴儿血斑DNA进行的桑格测序证实了这两个变异以复合杂合形式的遗传。我们展示了在没有患病患者的情况下通过外显子组测序实现诊断的首个案例。此外,这些数据支持了与钴胺素缺乏相关的潜在双基因遗传的可能性。