Abstract：
Genomes are inherently unstable and require constant DNA repair to maintain their genetic information. However, selective pressure has optimized repair mechanisms in somatic cells only to allow transmitting genetic information to the next generation, not to maximize sequence integrity long beyond the reproductive age. Recent studies have confirmed that somatic mutations, due to errors during genome repair and replication, accumulate in tissues and organs of humans and model organisms. Here, we describe recent advances in the quantitative analysis of somatic mutations in vivo. We also review evidence for or against a possible causal role of somatic mutations in aging. Finally, we discuss options to prevent, delay or eliminate de novo, random somatic mutations as a cause of aging.
摘要：
基因组本质上是不稳定的，需要不断的DNA修复来维持其遗传信息。然而,选择性压力优化了体细胞的修复机制，只允许将遗传信息传递给下一代，不要在超过生育年龄的时间内最大化序列完整性。最近的研究证实，体细胞突变，由于基因组修复和复制过程中的错误，积累在人类和模型生物的组织和器官中。这里,我们描述了体内体细胞突变定量分析的最新进展。我们还回顾了支持或反对体细胞突变在衰老中可能的因果作用的证据。最后,我们讨论了预防的选择，延迟或消除从头，随机体细胞突变是衰老的原因。
