Neuron-Specific Mechanisms Control the Mitochondrial Regulator PGC-1a Article Swipe
Eric R. McGregor
,
Dylan C. Souder
,
Josef Clark
,
Timothy W. Rhoads
,
Kevin W. Elicieri
,
Mark Beasley
,
Darcie L. Moore
,
Rozalyn M. Anderson
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1093/geroni/igab046.3508
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1093/geroni/igab046.3508
Mitochondrial dysfunction has been proposed as a hallmark of the aging process. Specifically, as a function of aging, mitochondria appear to have decreased enzyme activity and respiratory capacity and increase reactive oxygen species production. Brain aging is associated with morphological and homeostatic changes, including alterations in brain size, cognitive impairment, and white and grey matter integrity. However, the causes of these changes remain an open and actively pursued field of study. The ubiquitously expressed transcriptional coactivator peroxisome proliferator-activated receptor gamma-coactivator 1 (PGC-1a) has been described as the master regulator of mitochondrial function. Despite the emerging connections between PGC-1a and disease vulnerability, the regulation of PGC-1a outside of the skeletal muscle, liver, and adipose tissue is not well defined. This is particularly true in the brain, where PGC-1a is enriched in neurons, and alterations in expression levels have been linked to neurodegenerative disorders. Here we report that astrocytes and neurons differ substantially in mitochondrial status and the transcript variants of PGC-1a expressed, including using a neuron-specific promoter. Taking advantage of the ability of the tau-kinase GSK-3b to influence PGC-1a expression, we investigate how transcript variants are differentially regulated in primary neurons and astrocytes. Neuronal PGC-1a responds robustly to GSK3b inhibition by lithium, switching the dominant promoter, leading to changes in isoform distribution and abundance, while astrocytes are refractory to lithium treatment. The data presented here highlight key mechanisms for neuron-specific metabolic regulation that are likely to be relevant to neurodegenerative diseases that have a link to mitochondrial dysfunction.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/geroni/igab046.3508
- https://academic.oup.com/innovateage/article-pdf/5/Supplement_1/974/43189356/igab046.3508.pdf
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
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All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4200358641Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1093/geroni/igab046.3508Digital Object Identifier
- Title
-
Neuron-Specific Mechanisms Control the Mitochondrial Regulator PGC-1aWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
-
2021Year of publication
- Publication date
-
2021-12-01Full publication date if available
- Authors
-
Eric R. McGregor, Dylan C. Souder, Josef Clark, Timothy W. Rhoads, Kevin W. Elicieri, Mark Beasley, Darcie L. Moore, Rozalyn M. AndersonList of authors in order
- Landing page
-
https://doi.org/10.1093/geroni/igab046.3508Publisher landing page
- PDF URL
-
https://academic.oup.com/innovateage/article-pdf/5/Supplement_1/974/43189356/igab046.3508.pdfDirect link to full text PDF
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YesWhether a free full text is available
- OA status
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goldOpen access status per OpenAlex
- OA URL
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https://academic.oup.com/innovateage/article-pdf/5/Supplement_1/974/43189356/igab046.3508.pdfDirect OA link when available
- Concepts
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Biology, Mitochondrion, Regulator, Mitochondrial biogenesis, Coactivator, Cell biology, Peroxisome proliferator-activated receptor, Neuroscience, Receptor, Transcription factor, Gene, GeneticsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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