GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327394/primary200OKTranscriptomicsDrosophila melanogasterExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327394GEOGSEfalseRNA sequencing data of Drosophila melanogaster intestinal stem cells across different age groups, with overexpression of E374A (ADAR mutant) and knockdown of Zn72d and ADARMaintaining tissue homeostasis necessitates the presence of stem cells capable of self-renewal and differentiation. However, stem cell functionality is known to deteriorate with age, although the precise mechanisms involved remain elusive. In this study, we reveal that adenosine deaminase acting on RNA (ADAR) curbs intestinal stem cell (ISC) proliferation via an RNA editing mechanism during gut regeneration and aging in Drosophila, mice, and humans. Notably, the absence of ADAR in Drosophila ISCs elicits an elevation in Insulin-MAPK signaling activities, ultimately resulting in ISC over-proliferation. Our further findings reveal that this ADAR activity is mediated by zinc-finger protein at 72D (Zn72D), an RNA-binding protein known to govern ADAR editing in vivo. This investigation provides valuable insights into the role of ADAR-mediated editing in the regulation of stem cell function during tissue regeneration and aging. Moreover, it underscores the importance of appropriate editing regulation in delaying the onset of natural aging processes.2026/07/01GSE327394GSM9656246GSM9656235GSM9656234GSM9656245GSM9656248GSM9656226GSM9656237GSM9656247GSM9656236GSM9656242GSM9656231GSM9656230GSM9656241GSM9656244GSM9656233GSM9656243GSM9656232GSM9656239GSM9656228GSM9656227GSM9656249GSM9656238GSM9656229GSM965624025244327394Drosophila melanogaster