Mice lacking BCAS1, a novel myelin-associated protein, display hypomyelination, schizophrenia-like abnormal behaviors, and upregulation of inflammatory genes in the brain
Abstract
The abnormal expression and function of myelin-related proteins contribute to nervous system dysfunction associated with neuropsychiatric disorders; however, the underlying mechanism of this remains unclear. We found here that breast carcinoma amplified sequence 1 (BCAS1), a basic protein abundant in the brain, was expressed specifically in oligodendrocytes and Schwann cells, and that its expression level was decreased by demyelination. This suggests that BCAS1 is a novel myelin-associated protein. BCAS1 knockout mice displayed schizophrenia-like behavioral abnormalities and a tendency toward reduced anxiety-like behaviors. Moreover, we found that the loss of BCAS1 specifically induced hypomyelination and the expression of inflammation-related genes in the brain. These observations provide a novel insight into the functional link between oligodendrocytes and inflammation and/or abnormal behaviors.
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BCAS1 identifies oligodendrocyte lineage cells in the stage of active myelin formation in development and regeneration.
“Brain-enriched myelin-associated protein 1 (BCAS1) identifies oligodendrocyte lineage cells in the stage of active myelin formation in development and regeneration.”
From BCAS1-positive oligodendrocytes enable efficient cortical remyelination in multiple sclerosis (2025) · cites this paper as [30]
BCAS1+ oligodendrocytes are Olig2+ but do not express markers of oligodendrocyte precursor cells (e.g. NG2) and mature oligodendrocytes (e.g. CC1 or p25/TTTP), representing an intermediate stage of oligodendrocyte differentiation.
“BCAS1+ oligodendrocytes are Olig2+ but do not express markers of oligodendrocyte precursor cells (e.g. NG2) and mature oligodendrocytes (e.g. CC1 or p25/TTTP), thus representing an intermediate stage of oligodendrocyte differentiation.”
From BCAS1-positive oligodendrocytes enable efficient cortical remyelination in multiple sclerosis (2025) · cites this paper as [30]
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Fard, M. K., van der Meer, F., Sánchez, P., Cantuti-Castelvetri, L., Mandad, S., Jäkel, S., Fornasiero, E. F., Schmitt, S., Ehrlich, M., Starost, L., et al. (2017) · Science Translational Medicine · doi:10.1126/scitranslmed.aam7816 · Cited by 247 · see citing works
“function of BCAS1 is unknown, but there is evidence that it interacts with the dynein light chain (19) and is required for brain function because its absence results in reduced anxiety and schizophrenia-like behavioral abnormalities in mice (20).”
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BCAS1-positive oligodendrocytes enable efficient cortical remyelination in multiple sclerosis
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- Authors
- Ishimoto, T., Ninomiya, K., Inoue, R., Koike, M., Uchiyama, Y., & Mori, H.
- Affiliations
- University of Toyama (JP)
- Kyoto University (JP)
- Juntendo University (JP)
- Corresponding author
- Mori, Hisashi
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2017-02-23
- Volume
- 65
- Issue
- 5
- Pages
- 727-739
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2590623499
- Cited by
- 61
- References
- 7
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 8 · 2023: 6 · 2022: 7 · 2021: 10 · 2020: 7 · 2019: 6 · 2017: 3
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (16k01912, 15H01279, 16K01912)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- BCAS1, myelin-associated proteins, hypomyelination, oligodendrocytes, Schwann cells, demyelination, schizophrenia-like behavior, anxiety-like behavior, neuroinflammation, inflammatory gene expression, knockout mice, neuropsychiatric disorders
- MeSH terms
- Animals, Brain, Demyelinating Diseases, Myelin Basic Protein, Inflammation, Myelin Sheath, Neoplasm Proteins, Oligodendroglia, Schizophrenia, Transcriptional Activation, Up-Regulation, Mice, Knockout
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