A protein synthesis brake for hematopoietic stem cell maintenance

Genes Dev. 2022 Aug 1;36(15-16):871-873. doi: 10.1101/gad.350107.122.

Abstract

Bmi1 is essential for normal and leukemic hematopoiesis, but its target genes in hematopoietic stem cells (HSCs) are incompletely understood. In this issue of Genes & Development, Burgess et al. (pp. 887-900) demonstrate a novel role of Bmi1 in regulating ribosome biogenesis and protein synthesis. Bmi1-deficient HSCs exhibited reduced transplantability, with the up-regulation of ARX and genes involved in ribosome biogenesis. However, depletion of ARX or its known targets, p16 Ink4a /p19 Arf , only partially rescues Bmi1 loss-induced hematopoietic defects. They further demonstrate an increased protein synthesis rate and resultant proteostatic stress in Bmi1 -/- HSCs, indicating a novel mechanism by which Bmi1 controls HSC maintenance.

Keywords: polycomb; self-renewal; senescence; tissue regeneration; tumor suppressor.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Hematopoiesis / genetics
  • Hematopoietic Stem Cells / metabolism
  • Polycomb Repressive Complex 1* / genetics
  • Polycomb Repressive Complex 1* / metabolism
  • Proto-Oncogene Proteins* / metabolism

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • Proto-Oncogene Proteins
  • Polycomb Repressive Complex 1