酵母TEL1基因在抑制A-T细胞的高重组率、辐射诱导的细胞凋亡和端粒缩短方面可部分替代人类ATM基因。
The yeast TEL1 gene partially substitutes for human ATM in suppressing hyperrecombination, radiation-induced apoptosis and telomere shortening in A-T cells.
作者信息
Fritz E, Friedl A A, Zwacka R M, Eckardt-Schupp F, Meyn M S
机构信息
GSF, National Research Center for Environment and Health, Institute of Radiobiology, Neuherberg, Germany.
出版信息
Mol Biol Cell. 2000 Aug;11(8):2605-16. doi: 10.1091/mbc.11.8.2605.
Homozygous mutations in the human ATM gene lead to a pleiotropic clinical phenotype of ataxia-telangiectasia (A-T) patients and correlating cellular deficiencies in cells derived from A-T donors. Saccharomyces cerevisiae tel1 mutants lacking Tel1p, which is the closest sequence homologue to the ATM protein, share some of the cellular defects with A-T. Through genetic complementation of A-T cells with the yeast TEL1 gene, we provide evidence that Tel1p can partially compensate for ATM in suppressing hyperrecombination, radiation-induced apoptosis, and telomere shortening. Complementation appears to be independent of p53 activation. The data provided suggest that TEL1 is a functional homologue of human ATM in yeast, and they help to elucidate different cellular and biochemical pathways in human cells regulated by the ATM protein.
人类 ATM 基因的纯合突变会导致共济失调毛细血管扩张症（A-T）患者出现多效性临床表型，并使源自 A-T 供体的细胞出现相关细胞缺陷。酿酒酵母 tel1 突变体缺乏与 ATM 蛋白序列最相似的 Tel1p，与 A-T 存在一些共同的细胞缺陷。通过用酵母 TEL1 基因对 A-T 细胞进行基因互补，我们提供了证据表明 Tel1p 在抑制高频率重组、辐射诱导的细胞凋亡和端粒缩短方面可以部分补偿 ATM。互补作用似乎与 p53 激活无关。所提供的数据表明 TEL1 是酵母中人类 ATM 的功能同源物，有助于阐明人类细胞中由 ATM 蛋白调控的不同细胞和生化途径。
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