Signature changes in the expressions of protein-coding genes, lncRNAs, and repeat elements in early and late cellular senescence

Signature changes in the expressions of protein-coding genes, lncRNAs, and repeat elements in early and late cellular senescence

Replicative cellular senescence is the main cause of aging. It is important to note that early senescence is linked to tissueregeneration, whereas late senescence is known to trigger a chronically inflammatory phenotype. Despite the presence of variousgenome-wide studies, there is a lack of information on distinguishing early and late senescent phenotypes at the transcriptome level.Particularly, the changes in the noncoding RNA portion of the aging cell have not been fully elucidated. By utilising RNA sequencingdata of fibroblasts, hereby, we are not only reporting changes in gene expression profiles and relevant biological processes in the earlyand late senescent phenotypes but also presenting significant differences in the expressions of many unravelled long noncoding RNAs(lncRNAs) and transcripts arisen from repetitive DNA. Our results indicate that, in addition to previously reported L1 elements, variousLTR and DNA transposons, as well as members of the classical satellites including HSAT5 and α-satellites (ALR/Alpha), are expressedat higher levels in late senescence. Moreover, we revealed finer links between the expression levels of repeats with the genes locatednear them and known to be involved in cell cycle and senescence. Noncoding elements reported here provide a new perspective to beexplored in further experimental studies.

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