ArticleJournal of cell science2021
An SNX10-dependent mechanism downregulates fusion between mature osteoclasts.
Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- The molecular and functional interplay between the osteopetrosis-associated proteins SNX10, OSTM1, and CLC-7 during mouse osteoclastogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Elevated surface La promotes hyperfusion and contributes to impaired resorption in osteopetrosis.bioRxiv : the preprint server for biology · 2025Article
- Sorting nexin 10 regulates lysosomal ionic homeostasis via ClC-7 by controlling PI(3,5)P2.The Journal of cell biology · 2025Article
- SNX10 Is Involved in Ovarian Cancer Cell Metastasis by Repolarizing Tumor-Associated Macrophages Through mTOR1/Lysosomes Pathway.Biomedicines · 2025Article
- Cell-cell fusion: To lose one life and begin another.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- SNX10 in autosomal recessive osteosclerosis, osteosarcoma, rheumatoid arthritis, and osteoporosis: molecular mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Structure and function of the membrane microdomains in osteoclasts.Bone research · 2023Review
- Molecular Mechanisms of Craniofacial and Dental Abnormalities in Osteopetrosis.International journal of molecular sciences · 2023Review
- Genome sequencing identifies a large non-coding region deletion of SNX10 causing autosomal recessive osteopetrosis.Journal of human genetics · 2023Article
- Cell surface-bound La protein regulates the cell fusion stage of osteoclastogenesis.Nature communications · 2023Article
- Sorting Nexin 10 as a Key Regulator of Membrane Trafficking in Bone-Resorbing Osteoclasts: Lessons Learned From Osteopetrosis.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homozygosity for the R51Q mutation in sorting nexin 10 (SNX10) inactivates osteoclasts (OCLs) and induces autosomal recessive osteopetrosis in humans and in mice. We show here that the fusion of wild-type murine monocytes to form OCLs is highly regulated, and that its extent is limited by blocking fusion between mature OCLs. In contrast, monocytes from homozygous R51Q SNX10 mice fuse uncontrollably, forming giant dysfunctional OCLs that can become 10- to 100-fold larger than their wild-type counterparts. Furthermore, mutant OCLs display reduced endocytotic activity, suggesting that their deregulated fusion is due to alterations in membrane homeostasis caused by loss of SNX10 function. This is supported by the finding that the R51Q SNX10 protein is unstable and exhibits altered lipid-binding properties, and is consistent with a key role for SNX10 in vesicular trafficking. We propose that OCL size and functionality are regulated by a cell-autonomous SNX10-dependent mechanism that downregulates fusion between mature OCLs. The R51Q mutation abolishes this regulatory activity, leading to excessive fusion, loss of bone resorption capacity and, consequently, to an osteopetrotic phenotype in vivo. This article has an associated First Person interview with the joint first authors of the paper.
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Registered trials
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