外源性引入人或小鼠亚染色体片段对共济失调-毛细血管扩张细胞缺陷的表型校正。

Y Ejima, M S Sasaki
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引用次数: 2

摘要

一个含有人类11q22-23片段(包括ATM位点)的人-鼠杂交体被用来检测其纠正共济失调-毛细血管扩张(A- t)细胞缺陷的能力。对21个a - t来源杂交种的检测表明,在11q22-23片段完整转移的克隆中观察到获得性辐射抗性,而在供体来源11q片段丢失的克隆中则没有。在一个例外的克隆中,ATM位点被从转移的片段中删除,而它仍然部分具有辐射抗性。这个部分耐辐射的克隆被发现包括含有Atm基因的小鼠来源片段,这是人类Atm基因的小鼠同源物。在另外三个杂交种中观察到部分辐射抗性与小鼠Atm基因的存在相似的关联。结果表明,含有Atm基因的小鼠亚染色体片段和含有Atm基因的人11q22-23片段都能纠正细胞a - t缺陷,但前者的纠正程度明显较弱。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Phenotypic correction of ataxia-telangiectasia cellular defect by exogenously introduced human or mouse subchromosomal fragments.

A human-mouse hybrid containing a human 11q22-23 fragment including the ATM locus was used to examine its capability to correct the cellular defect of ataxia-telangiectasia (A-T). Examination of 21 A-T-derived hybrids indicated that the acquired radioresistance was observed in the clones where the 11q22-23 fragment was transferred intact, but not in those where donor-derived 11q segment was lost. In one exceptional clone, the ATM locus was deleted from the transferred fragment, while it was still partially radioresistant. This partially radioresistant clone was found to include the mouse-derived fragment containing the Atm gene, the mouse homologue of human ATM gene. Similar association of partial radioresistance with the presence of mouse Atm gene was observed in three additional hybrids. The results indicate that the cellular A-T defect can be corrected by the mouse subchromosomal fragment containing the Atm gene as well as by the human 11q22-23 fragment containing the ATM gene, but apparently to a lesser extent in the former.

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