Unintended targeting of Dmp1-Cre reveals a critical role for Bmpr1a signaling in the gastrointestinal mesenchyme of adult mice
Open accessAbstract
Cre/loxP technology has been widely used to study cell type-specific functions of genes. Proper interpretation of such data critically depends on a clear understanding of the tissue specificity of Cre expression. The Dmp1-Cre mouse, expressing Cre from a 14-kb DNA fragment of the mouse Dmp1 gene, has become a common tool for studying gene function in osteocytes, but the presumed cell specificity is yet to be fully established. By using the Ai9 reporter line that expresses a red fluorescent protein upon Cre recombination, we find that in 2-month-old mice, Dmp1-Cre targets not only osteocytes within the bone matrix but also osteoblasts on the bone surface and preosteoblasts at the metaphyseal chondro-osseous junction. In the bone marrow, Cre activity is evident in certain stromal cells adjacent to the blood vessels, but not in adipocytes. Outside the skeleton, Dmp1-Cre marks not only the skeletal muscle fibers, certain cells in the cerebellum and the hindbrain but also gastric and intestinal mesenchymal cells that express Pdgfra. Confirming the utility of Dmp1-Cre in the gastrointestinal mesenchyme, deletion of Bmpr1a with Dmp1-Cre causes numerous large polyps along the gastrointestinal tract, consistent with prior work involving inhibition of BMP signaling. Thus, caution needs to be exercised when using Dmp1-Cre because it targets not only the osteoblast lineage at an earlier stage than previously appreciated, but also a number of non-skeletal cell types.
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Conditional deletion of RANKL expression under the more specific SOST promoter generated a phenotype resembling the previous one, with a significant decrease in osteoclasts number in cancellous bone.
“As the activation of Dmp1-Cre promoters is not exclusive to osteocytes,53 the conditional deletion of RANKL expression was performed under the control of the more specific SOST promoter. This conditional deletion generated a phenotype resembling the previous one, with a significant decrease in osteoclasts number in cancellous bone.54”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [53]
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- Authors
- Lim, J., Burclaff, J., He, G., Mills, J. C., & Long, F.
- Affiliations
- Washington University in St. Louis (US)
- Central South University (CN)
- Corresponding author
- Long, Fanxin
- Venue
- Bone Research
- Published
- 2017-01-31
- Volume
- 5
- Issue
- 1
- Pages
- 16049-16049
- ISSN
- 2095-4700 (ISSN-L)
- 2095-6231
- PMC
- PMC5282469
- OpenAlex
- W2583781574
- Cited by
- 86
- References
- 26
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 9 · 2023: 16 · 2022: 10 · 2021: 4 · 2020: 11 · 2019: 11 · 2018: 8 · 2017: 4
- FWCI
- 3.80
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Bone Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by)
- Funders
- Alvin J. Siteman Cancer Center (DK105129, DK094989)
- Hope Center for Neurological Disorders (S10 RR0227552)
- National Institutes of Health (S10-RR0227552, DK-052574, DK105129)
- National Institute of General Medical Sciences (GM: 007067, T32GM007067)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK079333, R01DK094989, R01DK105129, P30DK052574)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR055923, R01AR060456)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › CRISPR and Genetic Engineering
- Keywords
- Cre-loxP recombination, BMPR1A, BMP signaling, osteocytes, osteoblasts, preosteoblasts, chondro-osseous junction, mesenchymal stem cells, PDGFRA, polyps, skeletal muscle, cerebellum, hindbrain
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