Autophagy is essential for oligodendrocyte differentiation, survival, and proper myelination
Abstract
Deficient myelination, the spiral wrapping of highly specialized membrane around axons, causes severe neurological disorders. Maturation of oligodendrocyte progenitor cells (OPC) to myelinating oligodendrocytes (OL), the sole providers of central nervous system (CNS) myelin, is tightly regulated and involves extensive morphological changes. Here, we present evidence that autophagy, the targeted isolation of cytoplasm and organelles by the double‐membrane autophagosome for lysosomal degradation, is essential for OPC/OL differentiation, survival, and proper myelin development. A marked increase in autophagic activity coincides with OL differentiation, with OL processes having the greatest increase in autophagic flux. Multiple lines of evidence indicate that autophagosomes form in developing myelin sheathes before trafficking from myelin to the OL soma. Mice with conditional OPC/OL‐specific deletion of the essential autophagy gene Atg5 beginning on postnatal Day 5 develop a rapid tremor and die around postnatal Day 12. Further analysis revealed apoptotic death of OPCs, reduced differentiation, and reduced myelination. Surviving Atg5−/− OLs failed to produce proper myelin structure. In vitro, pharmacological inhibition of autophagy in OPC/dorsal root ganglion (DRG) co‐cultures blocked myelination, producing OLs surrounded by many short processes. Conversely, autophagy stimulation enhanced myelination. These results implicate autophagy as a key regulator of OPC survival, maturation, and proper myelination. Autophagy may provide an attractive target to promote both OL survival and subsequent myelin repair after injury.
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During every round of mitosis, lysosomes must degrade approximately 140 proteins, and disruption of lysosomal function leads to prolonged mitotic timing and mitotic errors.
“During every round of mitosis, lysosomes must degrade approximately 140 proteins, and the disruption of lysosomal function leads to prolonged mitotic timing and mitotic errors.15”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [15]
Optimal cell division and development rely on functional lysosomes.
“Starting from the earliest embryonic stage, optimal cell division and development rely on functional lysosomes.”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [15]
Autophagic activity increases during progenitor cell differentiation into mature oligodendrocytes.
“Autophagic activity increases during progenitor cell differentiation into mature oligodendrocytes [444].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [444]
Conditional oligodendrocyte-specific deletion of Atg5 in mice leads to incomplete differentiation, reduced myelination, abnormal myelin compaction, oligodendrocytic death, and shortened life span.
“Conditional oligodendrocyte-specific deletion of Atg5 in mice leads to incomplete differentiation, reduced myelination, abnormal myelin compaction, oligodendrocytic death, and shortened life span [444].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [444]
During OPC differentiation, autophagy becomes most active in distal OPC processes, and autophagosomes are trafficked proximally to the soma in a manner similar to neurons.
“During oligodendroglial precursor (OPC) differentiation, autophagy becomes most active in distal OPC processes, and autophagosomes are trafficked proximally to the soma in a manner similar to neurons [444].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [444]
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- Authors
- Bankston, A. N., Forston, M. D., Howard, R. M., Andres, K. R., Smith, A. E., Ohri, S. S., Bates, M. L., Bunge, M. B., & Whittemore, S. R.
- Affiliations
- University of Louisville (US)
- University of Miami (US)
- Corresponding author
- Whittemore, Scott R.
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2019-06-04
- Volume
- 67
- Issue
- 9
- Pages
- 1745-1759
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2948615623
- Cited by
- 112
- References
- 62
- Citations by year
- 2026: 13 · 2025: 15 · 2024: 17 · 2023: 22 · 2022: 17 · 2021: 16 · 2020: 9 · 2019: 3
- FWCI
- 8.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (P30GM103507, R01NS009923, R01NS045734, R01NS054708, R01NS073584)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- autophagy, oligodendrocyte differentiation, myelination, oligodendrocyte precursor cells, ATG5, autophagosomes, oligodendrocyte survival, apoptosis, myelin sheath, dorsal root ganglia, remyelination, central nervous system myelin
- MeSH terms
- Autophagy-Related Protein 5, Oligodendrocyte Precursor Cells, Animals, Autophagy, Cell Survival, Cells, Cultured, Cerebral Cortex, Female, Ganglia, Spinal, Male, Mice, Inbred C57BL, Mice, Transgenic, Oligodendroglia, Rats, Sprague-Dawley, Coculture Techniques, Neurogenesis
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