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小鼠 H-2(da)和 H-2(db)的 H-2 丢失突变之间的关系。

The relationship between theH-2 loss mutations ofH-2(da) andH-2 (db) in the mouse.

机构信息

Department of Medicine, Austin Hospital, 3084, Heidelberg, Victoria, Australia.

出版信息

Immunogenetics. 1978 Dec;7(1):247-58. doi: 10.1007/BF01844012.

Abstract

The mouse strain B10.D2-H-2(da) carries the mutantH-2(da) allele, derived after chemical induction, and this has been shown to be a gain and loss mutation involving theH-2D(d) locus.BALB/c- H-2(db), derived spontaneously, is a loss mutation only, and appears not to involve theH-2D(d), but rather theH-2L(d) locus. The two mutations effectboth graft rejection and serologically detected H-2 specificities (Type II mutation). In the experiments described in this study, theloss mutations in theH-2(da) andH-2(db) mutants have been compared by skin grafting, and by direct and absorption serological techniques: (1) By skin grafting, using the well established complementation method, it has been shown thatH-2(da) andH-2(db) do not complement each other, i.e., the mutation in both occurred at the same 'locus.' However, by appropriate selection of donor and recipient, it has become clear thatH-2(da) had a greater loss than didH-2(db), althoughH-2(da) includes the loss found inH-2(db). (2) Serological studies have demonstrated that H-2D.4 was altered inH-2(da), but not inH-2(db); 'H-2.28' (detected by D-28b and D-29) was decreased or lost in both mutants;H-2(db) anti-BALB/c failed to react withH-2(da); both mutants reacted similarly with D-28 sera. In addition, sera made usingH-2(da) as donor did not contain an anti-H 2.28 antibody. The loss mutation involvingH-2(da) therefore appears to have led also to the loss of H-2.28 as found inH-2(db). We conclude that theH-2(da) strain arose after a complex mutation or recombination event which involvedboth theH-2D(d) locus and the closely linkedH-2L(d) locus, whereasH-2(db) affects only theH-2L locus.

摘要

B10.D2-H-2(da) 品系的小鼠携带经化学诱导产生的突变体 H-2(da) 等位基因,该突变被证实是涉及 H-2D(d) 基因座的增益和缺失突变。BALB/c-H-2(db) 是自发产生的缺失突变体,仅涉及 H-2L(d) 基因座,而不涉及 H-2D(d) 基因座。这两种突变均影响移植物排斥和血清学检测到的 H-2 特异性(II 型突变)。在本研究中描述的实验中,通过皮肤移植和直接和吸收血清学技术比较了 H-2(da) 和 H-2(db) 突变体中的缺失突变:(1) 通过皮肤移植,使用成熟的互补方法,已经表明 H-2(da) 和 H-2(db) 不能互补,即两个突变都发生在同一个“基因座”上。然而,通过适当选择供体和受体,可以清楚地看出,H-2(da) 的缺失程度大于 H-2(db),尽管 H-2(da) 包含了 H-2(db) 中的缺失。(2) 血清学研究表明,H-2D.4 在 H-2(da) 中发生改变,但在 H-2(db) 中没有;在两种突变体中,“H-2.28”(由 D-28b 和 D-29 检测到)减少或缺失;H-2(db) 抗 BALB/c 未能与 H-2(da) 反应;两种突变体与 D-28 血清反应相似。此外,使用 H-2(da) 作为供体产生的血清不含有抗 H 2.28 抗体。因此,涉及 H-2(da) 的缺失突变似乎也导致了与 H-2(db) 中发现的 H-2.28 缺失。我们得出结论,H-2(da) 品系是在涉及 H-2D(d) 基因座和紧密连锁的 H-2L(d) 基因座的复杂突变或重组事件后产生的,而 H-2(db) 仅影响 H-2L 基因座。

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