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DCAF13 Safeguards Hematopoietic Stem Cells via RRS1-Regulated Ribosome Biogenesis.

Mengke Li1, Yuxin Wu2, Shuai Zhou2

  • 1Institute of Hematology, Henan Key Laboratory of Stem Cell Differentiation and Modification, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|March 6, 2026
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Summary
This summary is machine-generated.

DCAF13 stabilizes RRS1, a key ribosome biogenesis factor, to maintain hematopoietic stem cell (HSC) function. Its deficiency causes HSC depletion and hematopoietic failure, revealing a critical DCAF13-RRS1 axis for blood production.

Keywords:
DCAF13HSCP53RRS1ribosome biogenesis

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Area of Science:

  • Hematology
  • Molecular Biology
  • Cell Biology

Background:

  • Hematopoietic stem cells (HSCs) are crucial for lifelong blood production.
  • HSC homeostasis relies on balancing self-renewal and differentiation.
  • The role of ribosome biogenesis in HSC regulation is not fully understood.

Purpose of the Study:

  • To identify novel regulators of HSC homeostasis.
  • To investigate the role of DCAF13 in HSC maintenance and ribosome biogenesis.
  • To elucidate the molecular mechanisms underlying DCAF13-mediated HSC regulation.

Main Methods:

  • Conditional deletion of Dcaf13 in murine hematopoietic cells.
  • Analysis of hematopoietic stem cell populations, blood counts, and survival rates.
  • Assessment of ribosome assembly, protein synthesis, and mRNA translation.
  • Investigation of DCAF13-RRS1 interaction and RRS1 ubiquitination.
  • Evaluation of p53 pathway activation and its role in Dcaf13-deficient mice.

Main Results:

  • Dcaf13 deletion led to severe pancytopenia, mortality, and HSC depletion.
  • DCAF13 deficiency disrupted ribosome assembly and protein synthesis, impacting myeloid and erythroid differentiation.
  • DCAF13 directly binds and stabilizes RRS1 via K27-linked polyubiquitination.
  • Dcaf13 deletion activated the p53 pathway, but p53 ablation only partially rescued HSC defects.

Conclusions:

  • DCAF13 is essential for HSC maintenance by stabilizing RRS1 and regulating ribosome biogenesis.
  • The DCAF13-RRS1 axis is critical for hematopoietic homeostasis.
  • This study provides insights into hematopoietic disorders and ribosomopathies.
  • Both p53-dependent and p53-independent mechanisms are involved in DCAF13-mediated HSC regulation.