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Related Concept Videos

Hematopoiesis01:21

Hematopoiesis

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The process of blood cell formation is called hematopoiesis. Hematopoiesis starts early during development, on the seventh day of embryogenesis. This phase of hematopoiesis is called the primitive wave, wherein the extraembryonic yolk sac allows the production of erythroid cells and endothelial cells from a common precursor called hemangioblast. The erythroid cells provide oxygen to support the growth of the rapidly dividing embryo. Hemangioblasts later develop into hematopoietic stem cells or...
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Hematopoiesis, or blood cell production, is a vital biological process that begins early in embryonic development and continues throughout life. This process generates the various types of cells found in blood, including red blood cells, white blood cells, and platelets from hematopoietic stem cells (HSCs).
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Regulation of Hematopoietic Stem Cells01:01

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Multipotency of Hematopoietic Stem Cells01:19

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The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...
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Ribosome profiling or ribo-sequencing is a deep sequencing technique that produces a snapshot of active translation in a cell. It selectively sequences the mRNAs protected by ribosomes to get an insight into a cell’s translation landscape at any given point in time.
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Ribosomal RNA Synthesis02:53

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Ribosome synthesis is a highly complex and coordinated process involving more than 200 assembly factors. The synthesis and processing of ribosomal components occurs not only in the nucleolus but also in the nucleoplasm and the cytoplasm of eukaryotic cells.
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Related Experiment Video

Updated: Jan 16, 2026

Mouse Fetal Liver Culture System to Dissect Target Gene Functions at the Early and Late Stages of Terminal Erythropoiesis
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RPS19 and RPL5 Haploinsufficient Models Reveal Divergent Ribosomal Subunit Controls of Fetal Hematopoiesis.

Lionel Blanc1, Yuefeng Tang2, Te Ling3

  • 1Feinstein Institute For Medical Research.

Research Square
|October 3, 2025
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Summary

Diamond Blackfan anemia syndrome (DBAS) results from ribosomal protein (RP) haploinsufficiency. Novel models reveal distinct RP functions in fetal blood development, impacting hematopoietic stem cells and erythroid production differently.

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Area of Science:

  • Hematology
  • Molecular Biology
  • Genetics

Background:

  • Diamond Blackfan anemia syndrome (DBAS) is a congenital ribosomopathy.
  • It arises from haploinsufficiency of ribosomal proteins (RPs).
  • The precise roles of RP stoichiometry and activity in erythroid development are unclear.

Purpose of the Study:

  • To investigate the divergent functions of small (RPS19) and large (RPL5) ribosomal subunit proteins in fetal hematopoiesis.
  • To elucidate the mechanisms underlying DBAS pathogenesis and clinical heterogeneity.

Main Methods:

  • Utilized novel in vivo models to study RPS19 and RPL5 haploinsufficiency.
  • Analyzed hematopoietic stem and progenitor cell (HSPC) dynamics.
  • Investigated p53-mediated cell death pathways (ferroptosis and apoptosis).
  • Assessed translational and transcriptional dysregulation, including RUNX1 expression.

Main Results:

  • RPL5 haploinsufficiency leads to HSPC accumulation and prenatal lethality via ferroptosis of erythroid progenitors.
  • RPS19 haploinsufficiency causes HSPC depletion and impaired erythroid expansion through apoptosis.
  • RPS19 deficiency results in translational/transcriptional dysregulation, including RUNX1 upregulation, mirroring human DBAS patients.
  • Runx1 deletion partially rescues HSPC numbers in RPS19-haploinsufficient mice.

Conclusions:

  • RPs from different ribosomal subunits have distinct roles in fetal hematopoiesis.
  • Imbalanced RP stoichiometry disrupts developmental programs, offering mechanistic insights into DBAS.
  • Findings explain the basis for DBAS clinical heterogeneity.