Zeng X, Winter D B, Kasmer C, Kraemer K H, Lehmann A R, Gearhart P J
Laboratory of Molecular Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Nat Immunol. 2001 Jun;2(6):537-41. doi: 10.1038/88740.
To determine whether DNA polymerase eta plays a role in the hypermutation of immunoglobulin variable genes, we examined the frequency and pattern of substitutions in variable VH6 genes from the peripheral blood lymphocytes of three patients with xeroderma pigmentosum variant disease, whose polymerase eta had genetic defects. The frequency of mutation was normal but the types of base changes were different: there was a decrease in mutations at A and T and a concomitant rise in mutations at G and C. We propose that more than one polymerase contributes to hypermutation and that if one is absent, others compensate. The data indicate that polymerase eta is involved in generating errors that occur predominantly at A and T and that another polymerase(s) may preferentially generate errors opposite G and C.
为了确定DNA聚合酶η是否在免疫球蛋白可变基因的高突变中发挥作用,我们检测了三名患有色素性干皮病变异型疾病患者外周血淋巴细胞中可变VH6基因的替代频率和模式,这些患者的聚合酶η存在基因缺陷。突变频率正常,但碱基变化类型不同:A和T处的突变减少,同时G和C处的突变增加。我们提出,不止一种聚合酶参与高突变,并且如果一种缺失,其他聚合酶会进行补偿。数据表明,聚合酶η参与产生主要发生在A和T处的错误,而另一种聚合酶可能优先产生与G和C相对的错误。