期刊:Science [American Association for the Advancement of Science (AAAS)] 日期:2020-12-31卷期号:371 (6524): 39.20-41
标识
DOI:10.1126/science.371.6524.39-t
摘要
Aging
Whereas cellular senescence is known to promote aging, many of the mechanisms controlling this process remain poorly understood. Using human mesenchymal precursor cells (hMPCs) carrying pathogenic mutations of the premature aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome, Wang et al. conducted a genome-wide CRISPR-Cas9–based screen to identify genes that could affect cellular senescence. They identified KAT7 , a histone acetyltransferase gene, as a driver of senescence in hMPCs. Inactivation of Kat7 in mice aging normally and in prematurely aging progeroid mice extended their life span. Although KAT7 requires further study in other cell types, these experiments highlight the value of genome-wide CRISPR-Cas9 screens and further illuminate the mechanisms controlling senescence.
Sci. Transl. Med. 13 , eabd2655 (2020).