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Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism
Open accessAbstract
The osteocyte, a terminally differentiated cell comprising 90%-95% of all bone cells, may have multiple functions, including acting as a mechanosensor in bone (re)modeling. Dentin matrix protein 1 (encoded by DMP1) is highly expressed in osteocytes and, when deleted in mice, results in a hypomineralized bone phenotype. We investigated the potential for this gene not only to direct skeletal mineralization but also to regulate phosphate (P(i)) homeostasis. Both Dmp1-null mice and individuals with a newly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting associated with elevated fibroblast growth factor 23 (FGF23) levels and normocalciuria. Mutational analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affecting the DMP1 start codon, and a second family carried a 7-bp deletion disrupting the highly conserved DMP1 C terminus. Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization. Our findings suggest a bone-renal axis that is central to guiding proper mineral metabolism.
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“Impaired DMP1 function is associated with a hypomineralized bone phenotype, which can result in rickets or osteomalacia 40,41 .”
From Sex-specific gene expression signatures of calcific aortic valve stenosis in a large collection of human tissues (2026) · cites this paper as [41]
In the citing paper
“Mutations in genes that have highly enriched expression in osteocytes cause rare bone and mineral disorders.”
From Osteocyte transcriptome mapping identifies a molecular landscape controlling skeletal homeostasis and susceptibility to skeletal disease (2021) · cites this paper as [20]
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Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23
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Self-citationPathogenic role of Fgf23 in Hyp mice
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Self-citationSix Genes Expressed in Bones and Teeth Encode the Current Members of the SIBLING Family of Proteins
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Hypophosphatemia: mouse model for human familial hypophosphatemic (vitamin D-resistant) rickets.
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MEPE, a New Gene Expressed in Bone Marrow and Tumors Causing Osteomalacia
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- Feng, J.Q. et al. The Dentin matrix protein 1 (Dmp1) is specifically expressed in mineralized, but not soft tissues during development. J. Dent. Res. 82, 776–780 (2003). · DOI
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Bonewald, L. F. (2011) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.320 · Cited by 2,287
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The Osteocyte: An Endocrine Cell … and More
Dallas, S. L., Prideaux, M., & Bonewald, L. F. (2013) · Endocrine Reviews · doi:10.1210/er.2012-1026 · Cited by 1,042
Self-citationFGF/FGFR signaling in health and disease
Xie, Y., Su, N., Yang, J., Tan, Q., Huang, S., Jin, M., Ni, Z., Zhang, B., Zhang, D., Luo, F., et al. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00222-7 · Cited by 904
“Both DMP1 and PHEX knockout mice exhibit hypophosphatemic rickets and increased FGF23 expression.(594,596) Although PHEX is a peptidase expressed in the bone, it can inhibit the expression FGF23 without regulating FGF23 degradation.”
BackgroundSelf-citation
Metadata
- Authors
- Feng, J. Q., Ward, L. M., Liu, S., Lu, Y., Xie, Y., Yuan, B., Yu, X., Rauch, F., Davis, S. I., Zhang, S., Rios, H., Drezner, M. K., Quarles, L. D., Bonewald, L. F., & White, K. E.
- Affiliations
- University of Missouri–Kansas City (US)
- University of Ottawa (CA)
- University of Kansas (US)
- University of Wisconsin–Madison (US)
- Indiana University Indianapolis (US)
- McGill University (CA)
- Corresponding author
- Ward, Leanne M
- Quarles, L Darryl
- ORCID
- Venue
- Nature Genetics
- Published
- 2006-10-08
- Volume
- 38
- Issue
- 11
- Pages
- 1310-1315
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC1839871
- OpenAlex
- W2051959338
- Cited by
- 1,199
- References
- 25
- Citations by year
- 2026: 29 · 2025: 19 · 2024: 31 · 2023: 47 · 2022: 60 · 2021: 59 · 2020: 61 · 2019: 63 · 2018: 62 · 2017: 57 · 2016: 52 · 2015: 64 · 2014: 58 · 2013: 81 · 2012: 93
- FWCI
- 46.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK063934, R01DK063934)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR045955, R01AR051587, AR 046798, R01AR027032, AR027032, R56AR045955, R56AR027032, P01AR046798, AR051587, AR-45955)
- National Institute of Dental and Craniofacial Research (DE 13480, R29DE013480)
- Topics
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Alkaline Phosphatase Research Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- DMP1, osteocytes, rickets, osteomalacia, phosphate homeostasis, fibroblast growth factor 23, bone mineralization, renal phosphate wasting, start codon mutation, C-terminal deletion
- MeSH terms
- Fibroblast Growth Factor-23, Adult, Animals, Bone and Bones, Calcification, Physiologic, Cells, Cultured, DNA Mutational Analysis, Female, Fibroblast Growth Factors, Humans, Kidney, Male, Mice, Inbred C57BL, Minerals, Osteocytes, Osteomalacia, Phosphates, Phosphoproteins, Rickets, Extracellular Matrix Proteins, Mice, Knockout, Mice
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