RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells - BIG - Biologie à Grande Échelle (BGE)
Article Dans Une Revue Nature Communications Année : 2023

RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells

Bigitha Bennychen
  • Fonction : Auteur
Annie Adrait
  • Fonction : Auteur
Yohann Couté
Mathieu Gabut

Résumé

Embryonic stem cell (ESC) fate decisions are regulated by a complex circuitry that coordinates gene expression at multiple levels from chromatin to mRNA processing. Recently, ribosome biogenesis and translation have emerged as key pathways that efficiently control stem cell homeostasis, yet the underlying molecular mechanisms remain largely unknown. Here, we identified RSL24D1 as highly expressed in both mouse and human pluripotent stem cells. RSL24D1 is associated with nuclear pre-ribosomes and is required for the biogenesis of 60S subunits in mouse ESCs. Interestingly, RSL24D1 depletion significantly impairs global translation, particularly of key pluripotency factors and of components from the Polycomb Repressive Complex 2 (PRC2). While having a moderate impact on differentiation, RSL24D1 depletion significantly alters ESC self-renewal and lineage commitment choices. Altogether, these results demonstrate that RSL24D1-dependant ribosome biogenesis is both required to sustain the expression of pluripotent transcriptional programs and to silence PRC2-regulated developmental programs, which concertedly dictate ESC homeostasis.
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Dates et versions

hal-04010880 , version 1 (25-05-2023)

Identifiants

Citer

Sébastien Durand, Marion Bruelle, Fleur Bourdelais, Bigitha Bennychen, Juliana Blin-Gonthier, et al.. RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells. Nature Communications, 2023, 14 (1), pp.356. ⟨10.1038/s41467-023-36037-7⟩. ⟨hal-04010880⟩
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