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首页> 外文期刊>Journal of Cellular Physiology >Telomerase activation in human fibroblasts during escape from crisis.
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Telomerase activation in human fibroblasts during escape from crisis.

机译：人类成纤维细胞中端粒酶的激活摆脱危机。

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The immortalization of human diploid fibroblasts requires the circumvention of both the senescence (M1) and crisis (M2) mechanisms of growth control. Cells expressing the SV40 T antigen virtually always bypass senescence, but only rarely escape crisis. The low frequency of this latter event indicates that cellular mutations are necessary to escape crisis. Thirteen subpopulations of T antigen-expressing human fibroblasts were cultured into crisis. Colonies that appeared to resume growth were assayed for telomerase activity, telomere maintenance, and the immortal phenotype. Our results show that 33 of 35 colonies were telomerase negative and were not immortal. Two colonies were telomerase positive when assayed in the first approximately 15 population doublings after crisis. The first was strongly positive, maintained telomeres at a stable short length, and was later determined to be immortal. The second initially had a weak telomerase signal, grew extremely slowly, and when examined had greatly elongated telomeres consistent with the ALT (alternative lengthening of telomeres) mechanism of telomere maintenance. These cells eventually grew faster and were later determined to be immortal. Additionally, two subpopulations had initially weak and later strong telomerase activity and the cells never entered a defined crisis period. We observed a perfect correlation between telomere maintenance and escape from crisis, supporting the hypothesis that the lack of stable telomeres causes crisis and that the ability to maintain telomeres abrogates crisis.
机译：人类不朽的二倍体成纤维细胞需要翻墙的衰老(M1)和危机(M2)的增长机制控制。几乎总是绕过衰老,但只有很少摆脱危机。后一个事件表明,细胞突变是必要的为了逃避危机。T的亚种群antigen-expressing人类成纤维细胞被培养成危机。似乎恢复增长是化验端粒酶活性,端粒维护和不朽的表型。35殖民地被端粒酶和负面的不是不朽的。积极的化验时第一个约危机后15个人口倍增。强烈积极,保持端粒稳定的短长度,后来决心是不朽的。端粒酶信号,增长极其缓慢,当检查大大延长端粒与ALT(替代延长一致端粒)的端粒维持机制。这些细胞最终增长速度和后来决心是不朽的。亚种群最初弱,后来强大的端粒酶活性和细胞没有进入了一个危机时期定义的。完美的端粒维持之间的相关性和摆脱危机,支持这一假说缺乏稳定端粒导致危机,维持端粒的功能废除危机。

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