Conserved exchange of paralog proteins during neuronal differentiation
Open accessPublished version of a preprint
Abstract
Gene duplication enables the emergence of new functions by lowering the evolutionary pressure that is posed on the ancestral genes. Previous studies have highlighted the role of specific paralog genes during cell differentiation, for example, in chromatin remodeling complexes. It remains unexplored whether similar mechanisms extend to other biological functions and whether the regulation of paralog genes is conserved across species. Here, we analyze the expression of paralogs across human tissues, during development and neuronal differentiation in fish, rodents and humans. Whereas ∼80% of paralog genes are co-regulated, a subset of paralogs shows divergent expression profiles, contributing to variability of protein complexes. We identify 78 substitutions of paralog pairs that occur during neuronal differentiation and are conserved across species. Among these, we highlight a substitution between the paralogs SEC23A and SEC23B members of the COPII complex. Altering the ratio between these two genes via RNAi-mediated knockdown is sufficient to influence neuron differentiation. We propose that remodeling of the vesicular transport system via paralog substitutions is an evolutionary conserved mechanism enabling neuronal differentiation.
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Cites
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- Authors
- Di Fraia, D., Anitei, M., Mackmull, M.-T., Parca, L., Behrendt, L., Andres-Pons, A., Gilmour, D., Helmer Citterich, M., Kaether, C., Beck, M., & Ori, A.
- Affiliations
- Leibniz Institute on Aging–Fritz Lipmann Institute, Jena, Germany
- Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) (DE)
- ETH Zurich (CH)
- University of Rome Tor Vergata (IT)
- European Molecular Biology Laboratory, Heidelberg, Germany
- University of Zurich (CH)
- Department of Biology, University of Tor Vergata, Rome, Italy
- Max Planck Institute of Biophysics (DE)
- Corresponding author
- Ori, Alessandro
- ORCID
- Venue
- Life Science Alliance
- Publisher
- Life Science Alliance, LLC
- Published
- 2022-03-10
- Volume
- 5
- Issue
- 6
- Pages
- e202201397
- ISSN
- 2575-1077 (ISSN-L)
- PMC
- PMC8917807
- OpenAlex
- W4226086748
- Cited by
- 2
- References
- 3
- Citations by year
- 2026: 2
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Life Science Alliance (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion, cc-by)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
- ETH Zürich Research Collection
- Funders
- Deutsche Forschungsgemeinschaft Research Training Group ProMoAge (GRK 2155)
- Else Kröner Fresenius Stiftung (2019_A79)
- Fritz-Thyssen Foundation (10.20.1.022MN)
- Chan Zuckerberg Initiative Neurodegeneration Challenge Network (2020-221617, 2021-230967)
- Deutsche Forschungsgemeinschaft (KA 1751/8-1)
- AIRC per la Ricerca sul Cancro (IG 23539)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- gene duplication, neuronal differentiation, SEC23A, SEC23B, COPII complex, vesicle trafficking, co-regulation, evolutionary conservation, chromatin remodeling, RNAi knockdown
- MeSH terms
- Animals, Biological Evolution, Gene Duplication
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