A genomics approach identifies senescence‐specific gene expression regulation

Aging Cell

Daniel H. Lackner¹  Makoto T. Hayashi¹  Anthony J. Cesare¹ 

[1] Salk Institute for Biological Studies, Molecular and Cell Biology Laboratory, La Jolla, CA, USA

关键词: replicative aging;    senescence;    DNA damage;    telomerase expression;    cell cycle;   

DOI  :  10.1111/acel.12234

来源: Wiley

【 摘 要 】

Summary

Replicative senescence is a fundamental tumor-suppressive mechanism triggered by telomere erosion that results in a permanent cell cycle arrest. To understand the impact of telomere shortening on gene expression, we analyzed the transcriptome of diploid human fibroblasts as they progressed toward and entered into senescence. We distinguished novel transcription regulation due to replicative senescence by comparing senescence-specific expression profiles to profiles from cells arrested by DNA damage or serum starvation. Only a small specific subset of genes was identified that was truly senescence-regulated and changes in gene expression were exacerbated from presenescent to senescent cells. The majority of gene expression regulation in replicative senescence was shown to occur due to telomere shortening, as exogenous telomerase activity reverted most of these changes.

【 授权许可】

CC BY   
© 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.