Open AccessA genomics approach identifies senescence‐specific gene expression regulation
Author(s) -
Lackner Daniel H.,
Hayashi Makoto T.,
Cesare Anthony J.,
Karlseder Jan
Publication year - 2014
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.12234
Subject(s) - telomere , senescence , biology , telomerase , transcriptome , gene , gene expression , microbiology and biotechnology , regulation of gene expression , dna damage , genetics , gene expression profiling , dna
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.