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Regulation of Telomere Length and Suppression of Genomic Instability in Human Somatic Cells by Ku86

机译：Ku86对人体细胞端粒长度的调节和基因组不稳定性的抑制

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Ku86 plays a key role in nonhomologous end joining in organisms as evolutionarily disparate as bacteria and humans. In eukaryotic cells, Ku86 has also been implicated in the regulation of telomere length although the effect of Ku86 mutations varies considerably between species. Indeed, telomeres either shorten significantly, shorten slightly, remain unchanged, or lengthen significantly in budding yeast, fission yeast, chicken cells, or plants, respectively, that are null for Ku86 expression. Thus, it has been unclear which model system is most relevant for humans. We demonstrate here that the functional inactivation of even a single allele of Ku86 in human somatic cells results in profound telomere loss, which is accompanied by an increase in chromosomal fusions, translocations, and genomic instability. Together, these experiments demonstrate that Ku86, separate from its role in nonhomologous end joining, performs the additional function in human somatic cells of suppressing genomic instability through the regulation of telomere length.
机译：Ku86在与细菌和人类进化上完全不同的生物体的非同源末端连接中起着关键作用。在真核细胞中，Ku86也参与了端粒长度的调控，尽管Ku86突变的影响在物种之间差异很大。实际上，端粒在不对Ku86表达无效的发芽酵母，裂变酵母，鸡细胞或植物中显着缩短，稍微缩短，保持不变或显着延长。因此，尚不清楚哪种模型系统与人类最相关。我们在这里证明，人类体细胞中Ku86的单个等位基因的功能失活会导致端粒大量丢失，并伴随着染色体融合，易位和基因组不稳定的增加。总之，这些实验表明，Ku86不同于其在非同源末端连接中的作用，在人类体细胞中还具有通过调节端粒长度来抑制基因组不稳定性的附加功能。

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