Ablation of the Sam68 RNA Binding Protein Protects Mice from Age-Related Bone Loss
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The Src substrate associated in mitosis of 68 kDa (Sam68) is a KH-type RNA binding protein that has been shown to regulate several aspects of RNA metabolism; however, its physiologic role has remained elusive. Herein we report the generation of Sam68-null mice by homologous recombination. Aged Sam68-/- mice preserved their bone mass, in sharp contrast with 12-month-old wild-type littermates in which bone mass was decreased up to approximately 75%. In fact, the bone volume of the 12-month-old Sam68-/- mice was virtually indistinguishable from that of 4-month-old wild-type or Sam68-/- mice. Sam68-/- bone marrow stromal cells had a differentiation advantage for the osteogenic pathway. Moreover, the knockdown of Sam68 using short hairpin RNA in the embryonic mesenchymal multipotential progenitor C3H10T1/2 cells resulted in more pronounced expression of the mature osteoblast marker osteocalcin when differentiation was induced with bone morphogenetic protein-2. Cultures of mouse embryo fibroblasts generated from Sam68+/+ and Sam68-/- littermates were induced to differentiate into adipocytes with culture medium containing pioglitazone and the Sam68-/- mouse embryo fibroblasts shown to have impaired adipocyte differentiation. Furthermore, in vivo it was shown that sections of bone from 12-month-old Sam68-/- mice had few marrow adipocytes compared with their age-matched wild-type littermate controls, which exhibited fatty bone marrow. Our findings identify endogenous Sam68 as a positive regulator of adipocyte differentiation and a negative regulator of osteoblast differentiation, which is consistent with Sam68 being a modulator of bone marrow mesenchymal cell differentiation, and hence bone metabolism, in aged mice.
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Germline Sam68-null mice have deficits of bone metabolism, sexual organ development, motor coordination and motor learning.
“Germline Sam68-null mice have deficits of bone metabolism, sexual organ development, motor coordination and motor learning95,96”
From The neurogenetics of alternative splicing (2016) · cites this paper as [95]
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- Authors
- Richard, S., Torabi, N., Franco, G. V., Tremblay, G. A., Chen, T., Vogel, G., Morel, M., Cléroux, P., Forget-Richard, A., Komarova, S., Tremblay, M. L., Li, W., Li, A., Gao, Y. J., & Henderson, J. E.
- Affiliations
- Jewish General Hospital (CA)
- Corresponding author
- Richard, Stéphane
- ORCID
- Venue
- PLoS Genetics
- Publisher
- Public Library of Science (PLoS)
- Published
- 2005-12-16
- Volume
- 1
- Issue
- 6
- Pages
- e74
- ISSN
- 1553-7390 (ISSN-L)
- 1553-7404
- PMC
- PMC1315279
- OpenAlex
- W2046002024
- Cited by
- 133
- References
- 66
- Citations by year
- 2026: 4 · 2024: 5 · 2023: 3 · 2022: 7 · 2021: 16 · 2020: 6 · 2019: 4 · 2018: 2 · 2017: 3 · 2016: 10 · 2015: 5 · 2014: 2 · 2013: 9 · 2012: 8
- FWCI
- 2.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Genetics (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship@McGill (McGill) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Canadian Institutes of Health Research (MT13377)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- Sam68, age-related bone loss, osteogenic differentiation, adipogenesis, mesenchymal stem cells, RNA metabolism, bone metabolism, osteocalcin, bone marrow adipocytes, mesenchymal progenitor cells
- MeSH terms
- Animals, Bone Marrow Cells, Cell Differentiation, DNA-Binding Proteins, Female, Fibroblasts, Humans, Male, Mice, Inbred C3H, Mice, Transgenic, Osteoblasts, Osteoporosis, Phosphoproteins, Recombination, Genetic, Osteocalcin, RNA-Binding Proteins, Adipocytes, Adaptor Proteins, Signal Transducing, Mice
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