ArticleScientific reports2016
Morc3 mutant mice exhibit reduced cortical area and thickness, accompanied by altered haematopoietic stem cells niche and bone cell differentiation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 40 citations in OpenAlex.
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- Emerging roles of the chromatin remodeler MORC2 in cancer metabolism.Medical oncology (Northwood, London, England) · 2024Review
- Adaptive introgression reveals the genetic basis of a sexually selected syndrome in wall lizards.Science advances · 2024Article
- Structural and functional validation of a highly specific Smurf2 inhibitor.Protein science : a publication of the Protein Society · 2024Article
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- Craniofacial dysmorphology in Down syndrome is caused by increased dosage of Dyrk1a and at least three other genes.Development (Cambridge, England) · 2023Article
- An intersectional analysis of LncRNAs and mRNAs reveals the potential therapeutic targets of Bi Zhong Xiao Decoction in collagen-induced arthritis rats.Chinese medicine · 2022Article
- 12-Deoxyphorbol-13-Hexadecanoate Abrogates OVX-Induced Bone Loss in Mice and OsteoclastogenesisFrontiers in pharmacology · 2022Article
- Microrchidia CW-Type Zinc Finger 2, a Chromatin Modifier in a Spectrum of Peripheral Neuropathies.Frontiers in cellular neuroscience · 2022Review
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- MORC protein family-related signature within human disease and cancer.Cell death & disease · 2021Review
- The role of MORC3 in silencing transposable elements in mouse embryonic stem cells.Epigenetics & chromatin · 2021Article
- Morc3 silences endogenous retroviruses by enabling Daxx-mediated histone H3.3 incorporation.Nature communications · 2021Article
- Integrating Transcriptome-Wide Association Study and mRNA Expression Profiling Identifies Novel Genes Associated With Osteonecrosis of the Femoral Head.Frontiers in genetics · 2021Article
- PKC-δ deficiency in B cells displays osteopenia accompanied with upregulation of RANKL expression and osteoclast-osteoblast uncoupling.Cell death & disease · 2020Article
- A 5-Gene Stemness Score for Rapid Determination of Risk in Multiple Myeloma.OncoTargets and therapy · 2020Article
- Mechanism for autoinhibition and activation of the MORC3 ATPase.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Advanced Genetic Approaches in Discovery and Characterization of Genes Involved With Osteoporosis in Mouse and Human.Frontiers in genetics · 2019Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Morc3, a member of a highly conserved nuclear matrix protein super-family plays an important part in chromatin remodeling, DNA repair, epigenetic regulation and cellular senescence. However, its role in bone homeostasis is not known. In the present study, a phenotype-driven ENU mouse mutagenesis screen revealed that Morc3(mut +/-) mice exhibit reduced cortical area and thickness with increased cortical porosity. Morc3(mut +/-) mice displayed reduced osteoclast numbers and surface per bone surface as well as osteocyte numbers, concomitant with altered gene expressions such as Rankl/Opg and Sost in ex vivo long bones. In vitro experiments revealed a significant increase in the number of Sca-1(+)/c-kit(+) haematopoietic stem cells (HSCs), and a significant reduction in senescence associated β-galactosidase activity in bone marrow macrophages (BMMs). In addition, we observed a decrease in osteoclastogenesis and bone resorption accompanied by upregulation of STAT1 expression in osteoclast lineage cells. Strikingly, Morc3 protein localization within the nuclear membrane was shifted to the cytoplasm in Morc3(mut +/-) osteoclasts. Further, Morc3(mut +/-) mice displayed increased osteoblast differentiation and altered gene expression. Collectively, our data show that Morc3 is a previously unreported regulator of cortical bone homeostasis and haematopoietic stem cells niche, accompanied by altered bone cell differentiation.
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