PUBLICATION

Estrogens regulate early embryonic development of the olfactory sensory system via estrogen-responsive glia

Authors
Takesono, A., Schirrmacher, P., Scott, A., Green, J.M., Lee, O., Winter, M.J., Kudoh, T., Tyler, C.R.
ID
ZDB-PUB-220114-6
Date
2022
Source
Development (Cambridge, England)   149(1): (Journal)
Registered Authors
Kudoh, Tetsuhiro, Lee, Okhyun, Tyler, Charles R.
Keywords
Embryogenesis, Endocrine disrupting chemicals, Olfactory glomerular development, Olfactory-mediated behaviour, Radial glia progenitor cells, Transgenic zebrafish embryo
MeSH Terms
  • Animals
  • Estrogen Receptor Antagonists/pharmacology
  • Estrogens/metabolism*
  • Fulvestrant/pharmacology
  • Neurogenesis*
  • Neuroglia/cytology*
  • Neuroglia/drug effects
  • Neuroglia/metabolism
  • Olfactory Bulb/cytology
  • Olfactory Bulb/drug effects
  • Olfactory Bulb/embryology*
  • Olfactory Receptor Neurons/cytology
  • Olfactory Receptor Neurons/metabolism
  • Receptors, Estrogen/antagonists & inhibitors
  • Synapses/metabolism
  • Synapses/physiology
  • Zebrafish
(all 17)
PubMed
35023540 Full text @ Development
Abstract
Estrogens are well-known to regulate development of sexual dimorphism of the brain; however, their role in embryonic brain development prior to sex-differentiation is unclear. Using estrogen biosensor zebrafish models, we found that estrogen activity in the embryonic brain occurs from early neurogenesis specifically in a type of glia in the olfactory bulb (OB), which we name estrogen-responsive olfactory bulb (EROB) cells. In response to estrogen, EROB cells overlay the outermost layer of the OB and interact tightly with olfactory sensory neurons at the olfactory glomeruli. Inhibiting estrogen activity using an estrogen receptor antagonist, ICI182,780 (ICI), and/or EROB cell ablation impedes olfactory glomerular development, including the topological organisation of olfactory glomeruli and inhibitory synaptogenesis in the OB. Furthermore, activation of estrogen signalling inhibits both intrinsic and olfaction-dependent neuronal activity in the OB, whereas ICI or EROB cell ablation results in the opposite effect on neuronal excitability. Altering the estrogen signalling disrupts olfaction-mediated behaviour in later larval stage. We propose that estrogens act on glia to regulate development of OB circuits, thereby modulating the local excitability in the OB and olfaction-mediated behaviour.
Genes / Markers
Marker Marker Type Name
cyp19a1bGENEcytochrome P450, family 19, subfamily A, polypeptide 1b
gap43GENEgrowth associated protein 43
mitfaGENEmelanocyte inducing transcription factor a
mpv17GENEmitochondrial inner membrane protein MPV17
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Figures
Figure Gallery (7 images)
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Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
a9
    		Complex
    as100TgTransgenic Insertion
      i149TgTransgenic Insertion
        i186TgTransgenic Insertion
          jf4TgTransgenic Insertion
            u300TgTransgenic Insertion
              uex3TgTransgenic Insertion
                w2
                  		Point Mutation
                  1 - 8 of 8
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                  Human Disease / Model
                  No data available
                  Sequence Targeting Reagents
                  No data available
                  Fish
                  No data available
                  Antibodies
                  Orthology
                  No data available
                  Engineered Foreign Genes
                  Marker Marker Type Name
                  GAL4EFGGAL4
                  GAL4FFEFGGAL4FF
                  GCaMPEFGGCaMP
                  GFPEFGGFP
                  mCherryEFGmCherry
                  NTREFGNTR
                  1 - 6 of 6
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                  Mapping
                  No data available
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                  Citation
                  Takesono, A., Schirrmacher, P., Scott, A., Green, J.M., Lee, O., Winter, M.J., Kudoh, T., Tyler, C.R. (2022) Estrogens regulate early embryonic development of the olfactory sensory system via estrogen-responsive glia. Development (Cambridge, England). 149(1):.