Papayannopoulou T, Lawn R M, Stamatoyannopoulos G, Maniatis T
Br J Haematol. 1982 Mar;50(3):387-99. doi: 10.1111/j.1365-2141.1982.tb01934.x.
Individuals heterozygous for the Greek (A gamma) variant of hereditary persistence of fetal haemoglobin (HPFH) synthesize Hb F whose gamma-globin chains are predominantly of the A gamma type. DNA obtained from Greek HPFH heterozygotes was used to test for abnormalities in the organization of non alpha-globin genes. In addition, gamma- and beta-globin expression was studied in BFUe cultures. Restriction endonuclease mapping showed that the G gamma, delta and beta genes in cis to the Greek HPFH determinant are intact. Overproduction of gamma-globin chains synthesis was observed in the BFUe cultures. A significant portion of the gamma chain synthesis was of the G gamma type, suggesting that the G gamma genes cis and trans to the HPFH chromosome are active in culture. DNA mapping data indicate that in contrast to G gamma A gamma HPFH and the G gamma (delta beta) thalassaemia, the Greek (A gamma) HPFH is not due to a large deletion in the non-alpha globin gene region. It is possible that the anomaly may result either from a small deletion or point mutation which influences non alpha-globin transcription. The in vitro synthesis data suggest that the low level of G gamma-globin chain synthesis in vivo is not the result of transcriptional inactivation of the G gamma gene, since this gene appears to be expressed in erythroid cell cultures. We speculate that the genetic lesion in Greek (A gamma) HPFH is in regulatory sequences which control the level of G gamma and A gamma expression during development.
遗传性胎儿血红蛋白持续存在(HPFH)希腊(Aγ)变异型的杂合子个体合成的Hb F,其γ珠蛋白链主要为Aγ型。从希腊HPFH杂合子获得的DNA用于检测非α珠蛋白基因组织的异常情况。此外,还在爆式红系集落形成单位(BFUe)培养物中研究了γ和β珠蛋白的表达。限制性内切酶图谱显示,与希腊HPFH决定簇顺式排列的Gγ、δ和β基因是完整的。在BFUe培养物中观察到γ珠蛋白链合成过量。γ链合成的很大一部分是Gγ型,这表明与HPFH染色体顺式和反式排列的Gγ基因在培养物中是活跃的。DNA图谱数据表明,与GγAγHPFH和Gγ(δβ)地中海贫血不同,希腊(Aγ)HPFH不是由于非α珠蛋白基因区域的大片段缺失所致。这种异常可能是由影响非α珠蛋白转录的小缺失或点突变引起的。体外合成数据表明,体内Gγ珠蛋白链合成水平低不是Gγ基因转录失活的结果,因为该基因在红系细胞培养物中似乎是表达的。我们推测,希腊(Aγ)HPFH的遗传损伤在于调控序列,这些序列在发育过程中控制Gγ和Aγ的表达水平。