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Although inhibition of  p16 INK4a   expression is critical to preserve the proliferative capacity of stem cells, the molecular mechanisms responsible for silencing  p16 INK4a   expression remain poorly characterized. Here, we show that the histone acetyltransferase (HAT) monocytic leukemia zinc finger protein (MOZ) controls the proliferation of both hematopoietic and neural stem cells by modulating the transcriptional repression of  p16 INK4a  . In the absence of the HAT activity of MOZ, expression of  p16 INK4a   is upregulated in progenitor and stem cells, inducing an early entrance into replicative senescence. Genetic deletion of  p16 INK4a   reverses the proliferative defect in both  Moz HAT  −  /  −   hematopoietic and neural progenitors. Our results suggest a critical requirement for MOZ HAT activity to silence  p16 INK4a   expression and to protect stem cells from early entrance into replicative senescence. S tem  C ells   2014;32:1591–1601

MOZ‐Mediated Repression of p16 INK 4 a Is Critical for the Self‐Renewal of Neural and Hematopoietic Stem Cells