Multi-omic phenotyping of iPSC-derived neurons harboring the MAPT V337M mutation reveals tau hypophosphorylation and perturbed axon morphology pathways Article Swipe
Gregory Mohl
,
Gary Dixon
,
Emily Marzette
,
Justin McKetney
,
Avi J. Samelson
,
Carlota Pereda Serras
,
Julianne Jin
,
Nabeela Ariqat
,
Andrew Li
,
Steven Boggess
,
Danielle L. Swaney
,
Martin Kampmann
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.06.04.597496
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.06.04.597496
Tau aggregation is a hallmark of several neurodegenerative diseases, including Alzheimer’s disease and frontotemporal dementia. There are disease-causing variants of the tau-encoding gene, MAPT , and the presence of tau aggregates is highly correlated with disease progression. However, the molecular mechanisms linking pathological tau to neuronal dysfunction are not well understood. This is in part due to an incomplete understanding of the normal functions of tau in development and aging, and how the associated molecular and cellular processes change in the context of causal disease variants of tau. To address these questions in an unbiased manner, we conducted multi-omic characterization of iPSC-derived neurons harboring the MAPT V337M mutation or MAPT knockdown. RNA-seq and phosphoproteomics revealed that both V337M mutation and tau knockdown perturbed levels of transcripts and phosphorylation of proteins related to axonogenesis or axon morphology. Surprisingly, we found that neurons with V337M tau had much lower tau phosphorylation than neurons with WT tau. Functional genomics screens uncovered regulators of tau phosphorylation in neurons and found that factors involved in axonogenesis modified tau phosphorylation in both MAPT WT and MAPT V337M neurons. Intriguingly, the p38 MAPK pathway specifically modified tau phosphorylation in MAPT V337M neurons. We propose that V337M tau perturbs tau phosphorylation and axon morphology pathways that are relevant to the normal function of tau, which could contribute to previously reported cognitive changes in preclinical MAPT variant carriers.
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- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2024.06.04.597496
- https://www.biorxiv.org/content/biorxiv/early/2024/06/06/2024.06.04.597496.full.pdf
- OA Status
- green
- Cited By
- 1
- References
- 86
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4399379159
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Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4399379159Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2024.06.04.597496Digital Object Identifier
- Title
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Multi-omic phenotyping of iPSC-derived neurons harboring the MAPT V337M mutation reveals tau hypophosphorylation and perturbed axon morphology pathwaysWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
- Publication date
-
2024-06-06Full publication date if available
- Authors
-
Gregory Mohl, Gary Dixon, Emily Marzette, Justin McKetney, Avi J. Samelson, Carlota Pereda Serras, Julianne Jin, Nabeela Ariqat, Andrew Li, Steven Boggess, Danielle L. Swaney, Martin KampmannList of authors in order
- Landing page
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https://doi.org/10.1101/2024.06.04.597496Publisher landing page
- PDF URL
-
https://www.biorxiv.org/content/biorxiv/early/2024/06/06/2024.06.04.597496.full.pdfDirect link to full text PDF
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-
YesWhether a free full text is available
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-
greenOpen access status per OpenAlex
- OA URL
-
https://www.biorxiv.org/content/biorxiv/early/2024/06/06/2024.06.04.597496.full.pdfDirect OA link when available
- Concepts
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Axon, Neuroscience, Morphology (biology), Mutation, Disease, Biology, Cell biology, Genetics, Internal medicine, Medicine, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
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1Total citation count in OpenAlex
- Citations by year (recent)
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2025: 1Per-year citation counts (last 5 years)
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86Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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