Cited by 295Neurogenesis and neuroplasticity mechanismsRetinoids in leukemia and cellular processesDevelopmental Biology and Gene Regulation

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Retinoic acid signaling and neuronal differentiation

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Janesick, Amanda, Wu, Stephanie Cherie, Blumberg, Bruce·2015·Cellular and Molecular Life Sciences

DOI 10.1007/s00018-014-1815-9PMC PMC11113123

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Abstract

The identification of neurological symptoms caused by vitamin A deficiency pointed to a critical, early developmental role of vitamin A and its metabolite, retinoic acid (RA). The ability of RA to induce post-mitotic, neural phenotypes in various stem cells, in vitro, served as early evidence that RA is involved in the switch between proliferation and differentiation. In vivo studies have expanded this "opposing signal" model, and the number of primary neurons an embryo develops is now known to depend critically on the levels and spatial distribution of RA. The proneural and neurogenic transcription factors that control the exit of neural progenitors from the cell cycle and allow primary neurons to develop are partly elucidated, but the downstream effectors of RA receptor (RAR) signaling (many of which are putative cell cycle regulators) remain largely unidentified. The molecular mechanisms underlying RA-induced primary neurogenesis in anamniote embryos are starting to be revealed; however, these data have been not been extended to amniote embryos. There is growing evidence that bona fide RARs are found in some mollusks and other invertebrates, but little is known about their necessity or functions in neurogenesis. One normal function of RA is to regulate the cell cycle to halt proliferation, and loss of RA signaling is associated with dedifferentiation and the development of cancer. Identifying the genes and pathways that mediate cell cycle exit downstream of RA will be critical for our understanding of how to target tumor differentiation. Overall, elucidating the molecular details of RAR-regulated neurogenesis will be decisive for developing and understanding neural proliferation-differentiation switches throughout development.

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See all 295

Authors: Janesick, A., Wu, S. C., & Blumberg, B.
Affiliations: University of California, Irvine (US)
Corresponding author: Blumberg, Bruce
ORCID: Janesick, Amanda
Wu, Stephanie Cherie
Blumberg, Bruce
Venue: Cellular and Molecular Life Sciences
Publisher: Springer Science and Business Media LLC
Published: 2015-01-06
Volume: 72
Issue: 8
Pages: 1559-1576
ISSN: 1420-682X (ISSN-L)
1420-9071
DOI: 10.1007/s00018-014-1815-9
PMC: PMC11113123
OpenAlex: W2117145998
Cited by: 295
References: 268
Citations by year: 2026: 15 · 2025: 37 · 2024: 30 · 2023: 36 · 2022: 25 · 2021: 44 · 2020: 31 · 2019: 24 · 2018: 22 · 2017: 16 · 2016: 13 · 2015: 2
FWCI: 2.22
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Cellular and Molecular Life Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
eScholarship (California Digital Library) (submittedVersion)
eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
Funders: National Science Foundation
Topics: Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Keywords: retinoic acid signaling, neuronal differentiation, primary neurogenesis, retinoic acid receptor, proneural transcription factors, vitamin A deficiency, dedifferentiation, tumor differentiation
MeSH terms: Animals, Antigens, Neoplasm, Antineoplastic Agents, Humans, Neoplasms, Neurons, Tretinoin, Signal Transduction, Receptors, Retinoic Acid, Cell Cycle Proteins, Neurogenesis

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