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A reduction in A-to-I RNA editing by ADAR disrupts Pumilio-mediated inhibition of MAPK signaling to drive intestinal stem cell aging
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DOI：10.1126/scisignal.aee6812.png)
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Abstract
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Intestinal stem cell (ISC) function declines with age, and ISC dysregulation is associated with shortened life span. Zhang et al. found that the RNA editing enzyme ADAR restrained ISC proliferation in fruit flies, and its abundance and activity decreased with aging and after gut injury. ISC-specific loss of ADAR in young flies caused intestinal hyperproliferation and reduced life span, whereas ADAR overexpression in aged flies improved gut function and increased life span. ADAR inhibited proliferative MAPK signaling in ISCs because its RNA editing activity generated a translational repressor of MAPK pathway components. Reductions in colonic ADAR2 and a protein that stabilizes it were associated with aging in humans and with intestinal regeneration in mice, suggesting that ADAR-mediated regulation of ISCs may be conserved. —Annalisa M. VanHook
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