B6.C-H-2bm12. A new H-2 mutation in the I region in the mouse
B6.C-H-2bm12. A new H-2 mutation in the I region in the mouse
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B6.C-H-2bm12。
DOI：
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发表时间：
1979
影响因子：
15.3
通讯作者：
Australia
中科院分区：
文献类型：
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作者：
I. Mckenzie;G. Morgan;M. Sandrin;R. W. Michaelides;Melvold;H. Kohn;Australia
描述了B6.C-H-2bm 12突变体，并提出了IA亚区突变位点的证据。该突变体是一种获得和丢失型突变体，平衡状态下的bm 12或由C57 BL/6移植物形成的bm 12在14-16 d内被排斥。通过使用H-2重组菌株的基因互补方法进行的作图研究将突变置于H-2复合物的K或IA区，此外，使用该试验和使用其他H-2突变体表明H-2Kb不是突变位点，使得IA区成为最可能的位点。通过细胞毒性、玫瑰花结和吸收分析，用一组H-2b、Iab和其他Ia血清进行血清学分析，表明H-2特异性没有改变，特别是H-2.K33。相比之下，由IA亚区编码的所有Iab特异性（Ia.3、8、9、15和可能的20）被广泛改变，并且不存在或在量上大大减少，这表明携带Ia的分子中的广泛改变。bm 12突变体在混合淋巴细胞反应（MLR）中强烈刺激亲本C57 BL/6菌株，并且还发生倒数，刺激程度与来源于另一H-2单倍型的K + IA差异相似，并指向影响Lad-1位点的突变。广泛的组织相容性变化的存在下，在血清学检测Ia特异性的显着改变，和一个强大的MLR，所有产生的一个突变，提供了强有力的证据的身份Ia-1，Lad-1，和H-2（IA）基因座在IA亚区。bm 12突变体在确定Ia特异性、Ir基因和受I区影响的其他现象之间的关系方面应该是有价值的。
The B6.C-H-2bm12 mutant is described and evidence is presented for the mutational site occurring in the IA subregion. The mutant is of the gain and loss type as bm12 in equilibrium or formed from C57BL/6 grafts are rejected in 14-16 d. Mapping studies by the gene-complementation method using H-2 recombinant strains place the mutation in the K or IA regions of the H-2 complex and furthermore, the use of this test and the use of other H-2 mutants indicate that H-2Kb is not the site of the mutation, making the IA region the most likely site. Serological analysis with a battery of H-2b, Iab, and other Ia sera, both by cytotoxicity, rosetting, and also by absorption analysis, indicated no alteration in H-2 specificities, particularly in H-2.K33. By contrast, all of the Iab specificities coded for by the IA subregion (Ia.3, 8, 9, 15, and possibly 20) are extensively altered and are either absent or greatly reduced in amount indicating an extensive alteration in the Ia- bearing molecule. The bm12 mutant strongly stimulates the parental C57BL/6 strain in an mixed lymphocyte reaction (MLR), and the reciprocal also occurs, the degree of stimulation being similar to that obtained with K + IA differences originating in another H-2 haplotype and points to the mutation effecting the Lad-1 locus. The presence of an extensive histocompatibility change, a marked alteration in the serologically detected Ia specificities, and a strong MLR, all produced by the one mutation, provides strong evidence for the identity of the Ia-1, Lad-1, and H-2(IA) loci in the IA subregion. The bm12 mutant should be of value in determining the relationship of Ia specificities, Ir genes, and other phenomena effected by the I region.