Rajan T V, Halay E D, Potter T A, Evans G A, Seidman J G, Margulies D H
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
EMBO J. 1983;2(9):1537-42. doi: 10.1002/j.1460-2075.1983.tb01620.x.
Variants that no longer express an entire H-2 haplotype were readily isolated, by immunoselection with antisera directed against the haplotype, from an H-2b/H-2d heterozygous Friend leukemia cell line carrying a Robertsonian translocation of the chromosomes bearing the H-2 genetic region. These variants can be denoted as being of the phenotype H-2b- H-2d+ or H-2b+ H-2d-. Some of the H-2b- H-2d+ variants: (1) lack the restriction enzyme fragments characteristic of the missing H-2b haplotype, as assessed by Southern blot analysis; (2) express more cell surface H-2d antigens than wild-type cells, as assessed by flow microfluorimetry; and (3) appear to have become homozygous for the more active H-2d-linked allele at the Glyoxalase I locus. These variants thus seem to have lost genetic material corresponding to the H-2b haplotype and may have gained genetic material corresponding to the H-2d haplotype. These results are consistent with the possibility that these variants were generated by mitotic recombination.
通过用针对该单倍型的抗血清进行免疫选择,很容易从携带H - 2基因区域染色体罗伯逊易位的H - 2b/H - 2d杂合性弗瑞德白血病细胞系中分离出不再表达完整H - 2单倍型的变体。这些变体可被标记为H - 2b - H - 2d +或H - 2b + H - 2d -表型。一些H - 2b - H - 2d +变体:(1)通过Southern印迹分析评估,缺乏缺失的H - 2b单倍型特征性的限制性酶切片段;(2)通过流式微量荧光测定法评估,表达比野生型细胞更多的细胞表面H - 2d抗原;(3)在乙二醛酶I位点似乎已成为更活跃的H - 2d连锁等位基因的纯合子。因此,这些变体似乎丢失了与H - 2b单倍型相对应的遗传物质,并且可能获得了与H - 2d单倍型相对应的遗传物质。这些结果与这些变体是由有丝分裂重组产生的可能性一致。