期刊
CELL
卷 182, 期 1, 页码 12-23出版社
CELL PRESS
DOI: 10.1016/j.cell.2020.06.024
关键词
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资金
- NIH [P01 AG017242, P01 AG047200, P30 AG038072, U01 ES029519, K99 AG056656]
- Glenn Foundation for Medical Research
- Shanghai Jiao Tong University School of Medicine
Age-related accumulation of postzygotic DNA mutations results in tissue genetic heterogeneity known as somatic mosaicism. Although implicated in aging as early as the 1950s, somatic mutations in normal tissue have been difficult to study because of their low allele fractions. With the recent emergence of cost-effective highthroughput sequencing down to the single-cell level, enormous progress has been made in our capability to quantitatively analyze somatic mutations in human tissue in relation to aging and disease. Here we first review how recent technological progress has opened up this field, providing the first broad sets of quantitative information on somatic mutations in vivo necessary to gain insight into their possible causal role in human aging and disease. We then propose three major mechanisms that can lead from accumulated de novo mutations across tissues to cell functional loss and human disease.
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