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Related Concept Videos

Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

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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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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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Commitment is the  process whereby stem cells:
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Hematopoiesis01:21

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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Combinatorial gene control is the synergistic action of several transcriptional factors to regulate the expression of a single gene. The absence of one or more of these factors may lead to a significant difference in the level of gene expression or repression.
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Polycomb repressive complex 2 component Suz12 is required for hematopoietic stem cell function and lymphopoiesis.

Stanley C W Lee1, Sarah Miller2, Craig Hyland2

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Polycomb repressive complex 2 (PRC2) is crucial for hematopoietic stem cell (HSC) maintenance. Its dosage impacts HSC self-renewal, with complete loss causing failure, while partial loss enhances it.

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Area of Science:

  • Epigenetics and Gene Regulation
  • Stem Cell Biology
  • Hematopoiesis

Background:

  • Polycomb repressive complex 2 (PRC2) is a key chromatin modifier regulating stem cell function.
  • Studies on PRC2 function are complex due to early embryonic lethality and functional redundancy between Ezh1 and Ezh2.

Purpose of the Study:

  • To investigate the role of PRC2 in hematopoiesis using conditional deletion of its core component, suppressor of zeste 12 protein homolog (Suz12).
  • To elucidate the dose-dependent effects of PRC2 on hematopoietic stem cells (HSCs) and mature blood cell lineages.

Main Methods:

  • Conditional deletion of the Suz12 gene in mice.
  • Analysis of hematopoietic stem cell maintenance and self-renewal.
  • Assessment of lymphoid and myeloid lineage development.

Main Results:

  • Complete loss of Suz12 led to a failure of hematopoiesis and loss of HSC maintenance in both embryonic and adult stages.
  • Partial loss of PRC2 activity resulted in enhanced HSC self-renewal.
  • Suz12 was essential for lymphoid development but dispensable for granulocytic, monocytic, and megakaryocytic cell development.

Conclusions:

  • PRC2 plays a multifaceted, dose-dependent role in hematopoiesis, impacting HSCs and distinct blood cell lineages differently.
  • Understanding these complex effects is critical for considering PRC2 as a therapeutic target in cancer, given its context-specific consequences.