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低白血病小鼠内源性鼠白血病病毒诱导中的基因相互作用

Genetic interactions in induction of endogenous murine leukemia virus from low leukemic mice.

作者信息

McCubrey J, Risser R

出版信息

Cell. 1982 Apr;28(4):881-8. doi: 10.1016/0092-8674(82)90067-8.

DOI:10.1016/0092-8674(82)90067-8
PMID:6284378
Abstract

The frequency of ecotropic murine leukemia virus (MuLV) production in cells induced with halogenated pyrimidines has been investigated in several low leukemic strains of mice. Very few BALB/c or C57BL/6 (B6) induced embryo cells produce MuLV; this low frequency increases 10 to 50 fold in cells of the BALB/c x B6 F1 hybrid. Data from back-crosses of the F1 hybrid to each parent and from BALB/c x B6 recombinant inbred strains indicate that the phenotype of enhanced MuLV production results from interaction of two unlinked loci, dominant (+/+) alleles of which are carried by either parent. Genetic tests with BALB/c x B6 recombinant inbred strains confirm this two-locus model. The loci are designated Inc-1 and Inb-1 to signify their phenotypic detection by induction and the BALB/c or B6 strain of origin, respectively. Examination of hybrids of BALB/c and of B6 with other strains indicates that strains related in pedigree to BALB/c carry Inc-1, whereas those related to B6 carry Inb-1. Identification of genetic loci that specifically interact to enhance MuLV production after exposure to halogenated pyrimidines indicates the existence of mechanisms that regulate the induction or intracellular expression of endogenous MuLV.

摘要

在几种低白血病小鼠品系中,研究了用卤代嘧啶诱导的细胞中嗜亲性鼠白血病病毒(MuLV)的产生频率。很少有BALB/c或C57BL/6(B6)诱导的胚胎细胞产生MuLV;在BALB/c×B6 F1杂种细胞中,这种低频率增加了10到50倍。F1杂种与每个亲本的回交数据以及BALB/c×B6重组近交系的数据表明,MuLV产生增强的表型是由两个不连锁的基因座相互作用导致的,其中一个亲本携带显性(+/+)等位基因。用BALB/c×B6重组近交系进行的遗传测试证实了这两个基因座模型。这两个基因座分别命名为Inc-1和Inb-1,以分别表示通过诱导和起源的BALB/c或B6品系对它们进行表型检测。对BALB/c和B6与其他品系的杂种的检查表明,谱系上与BALB/c相关的品系携带Inc-1,而与B6相关的品系携带Inb-1。鉴定在暴露于卤代嘧啶后特异性相互作用以增强MuLV产生的基因座,表明存在调节内源性MuLV诱导或细胞内表达的机制。

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