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Related Concept Videos

Bone Disorders01:29

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Related Experiment Video

Updated: Jan 13, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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Deletion of Dock7 Exons 3 and 4 Results in Reduced Trabecular Microarchitecture and a Decrease in Mineralization.

Talia Lizotte1, Conner Lajoie2, Sarah Porter1

  • 1Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, Biddeford, ME 04005, USA.

Biorxiv : the Preprint Server for Biology
|January 8, 2026
PubMed
Summary
This summary is machine-generated.

Dedicator of Cytokinesis 7 (DOCK7) gene exons 3-4 are crucial for maintaining healthy bone structure. Deleting these exons in mice significantly reduced bone volume and impaired osteoblast function, validating a new model for skeletal research.

Keywords:
BglapDock7boneosteoblasttrabecular bone

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Area of Science:

  • Skeletal Biology and Genetics
  • Cellular and Molecular Biology

Background:

  • Dedicator of Cytokinesis 7 (DOCK7) is implicated in skeletal homeostasis.
  • Existing DOCK7 mutant models lack tissue-specific deletion capabilities, hindering detailed study.

Purpose of the Study:

  • To validate a floxed DOCK7 allele for conditional gene deletion studies.
  • To characterize the skeletal phenotype of mice with global deletion of DOCK7 exons 3-4.

Main Methods:

  • Generation of Dock7em2/em2 mice with global deletion of DOCK7 exons 3-4.
  • Assessment of bone microarchitecture in male and female mice using micro-CT.
  • In vitro differentiation of bone marrow stromal cells (BMSCs) to evaluate osteoblast function.

Main Results:

  • Dock7em2/em2 mice showed reduced trabecular bone volume (30-37%) in the femur and vertebrae.
  • Cortical bone thickness remained unchanged, but sex-specific alterations in femoral area were observed.
  • Dock7em2/em2 BMSCs displayed reduced mineralization and decreased Bglap expression, indicating impaired osteoblast differentiation.

Conclusions:

  • DOCK7 exons 3-4 are essential for normal trabecular bone acquisition and osteoblast differentiation.
  • The Dock7em2/em2 mouse is a valid loss-of-function model for DOCK7.
  • This model serves as a foundation for future tissue-specific studies on DOCK7's role in bone biology.