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Updated: Feb 6, 2026

Isolation, Culture, and Differentiation of Bone Marrow Stromal Cells and Osteoclast Progenitors from Mice
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Schlafen2 mutation in mice causes an osteopetrotic phenotype due to a decrease in the number of osteoclast

Ibrahim Omar1, Gali Guterman-Ram2, Dolev Rahat3

  • 1The Lautenberg Center for Immunology and Cancer Research, The Biomedical Research Institute Israel Canada of the Faculty of Medicine, The Hebrew University Hadassah Medical School Jerusalem, Jerusalem, Israel.

Scientific Reports
|August 31, 2018
PubMed

Insights

The Schlafen (Slfn) gene family co-evolved with osteoclast genes. Loss of Slfn2 in mice leads to increased bone mass and fewer osteoclasts, suggesting Slfn2 is crucial for normal osteoclast differentiation.

Area of Science:

  • Bone Biology
  • Cellular and Molecular Medicine
  • Genetics and Genomics

Background:

  • Osteoclasts are key bone-resorbing cells derived from myeloid progenitors.
  • Molecular mechanisms regulating osteoclast progenitor homeostasis remain largely unknown.
  • Phylogenetic analysis revealed co-evolution of the Schlafen (Slfn) gene family with osteoclast-related genes.

Purpose of the Study:

  • To investigate the role of Schlafen (Slfn) gene family, specifically Slfn2, in osteoclast development and function.
  • To elucidate the molecular mechanisms governing osteoclast homeostasis.
  • To determine if Slfn2 deficiency impacts bone mass and osteoclast activity.

Main Methods:

  • Analysis of normalized phylogenetic profiles of the Schlafen (Slfn) gene family.
  • Utilized Slfn2 loss-of-function mutant mice (elektra).
  • Performed bone marrow monocyte cultures and assessed osteoclast differentiation and resorption, and quantified osteoclast precursor populations (CD11b-Ly6Chi).

Main Results:

  • Slfn2 loss-of-function mutant mice (Slfn2eka/eka) displayed significantly increased cancellous bone mass.
  • A profound reduction in osteoclast numbers and total resorption area was observed in Slfn2eka/eka mice.
  • Bone marrow from Slfn2eka/eka mice contained significantly fewer CD11b-Ly6Chi osteoclast precursors.

Conclusions:

  • Schlafen (Slfn)2 is essential for normal osteoclast differentiation and function.
  • Loss of Slfn2 function in mice results in an osteopetrotic phenotype.
  • Slfn2 plays a critical role in regulating osteoclast homeostasis and bone metabolism.

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