Wajcman H, Girodon E, Promé D, North M L, Plassa F, Duwig I, Kister J, Bergerat J P, Oberling F, Lampert E
INSERM U91, Hôpital Henri Mondor, Créteil, France.
Hum Genet. 1995 Dec;96(6):711-6. doi: 10.1007/BF00210304.
Hb Puttelange [beta 140(H18)Ala-->Val] was found as a de novo mutation in two siblings of a French family suffering from polycythemia. Both parents were phenotypically normal and exclusion of paternity has been ruled out by the study of several polymorphic markers located on different chromosomes. The structural modification of Hb Puttelange was established by reversed-phase HPLC analysis of the tryptic digest of the abnormal chain. The amino acid composition of an abnormal beta T14 peptide revealed that one of the four residues of Ala was replaced by a Val. Tandem mass spectrometry demonstrated that the substitution concerned position beta 140 (H18). This hemoglobin displays an increased oxygen affinity that is responsible for the polycythemia. De novo mutations, as demonstrated again in the case of this variant, have the highest probabilities of detection when they lead to pathological manifestations. They may result either from a somatic mutation in a very early stage of the embryological development of the propositus or may have a parental origin with occurrence of a germline mosaicism. The study of the beta-globin gene indicated that this case of Hb Puttelange probably arose from a mutation affecting a part of the germline of the father, therefore leading to a true recurrence risk.
血红蛋白普特拉朗日[β140(H18)丙氨酸→缬氨酸]是在一个患有红细胞增多症的法国家庭的两名同胞中发现的一种新发突变。父母双方表型正常,通过对位于不同染色体上的多个多态性标记的研究排除了父权争议。通过对异常链胰蛋白酶消化产物的反相高效液相色谱分析确定了血红蛋白普特拉朗日的结构修饰。异常βT14肽的氨基酸组成显示,四个丙氨酸残基中的一个被缬氨酸取代。串联质谱表明,该取代发生在β140(H18)位。这种血红蛋白显示出增加的氧亲和力,这是导致红细胞增多症的原因。新发突变,如该变体病例再次证明的那样,当它们导致病理表现时,检测到的概率最高。它们可能源于先证者胚胎发育早期的体细胞突变,或者可能有亲代来源,即发生了生殖系嵌合体。对β珠蛋白基因的研究表明,这种血红蛋白普特拉朗日病例可能源于影响父亲部分生殖系的突变,因此导致了真正的复发风险。