PUBLICATION

The gonadal soma controls ovarian follicle proliferation through Gsdf in zebrafish

Authors
Yan, Y.L., Desvignes, T., BreMiller, R., Wilson, C., Dillon, D., High, S., Draper, B., Buck, C.L., Postlethwait, J.
ID
ZDB-PUB-170901-4
Date
2017
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   246(11): 925-945 (Journal)
Registered Authors
BreMiller, Ruth, Desvignes, Thomas, Draper, Bruce, Postlethwait, John H., Wilson, Catherine, Yan, Yi-Lin
Keywords
BMP15, GDF9, Gonad development, Polycystic ovarian syndrome (PCOS), Sertoli cells, TGFβ, gonadal soma germ cell interaction, granulosa cells, insulin signaling, oogenesis, ovarian follicle
MeSH Terms
  • Adult Stem Cells/physiology*
  • Animals
  • Female
  • Gene Expression Regulation, Developmental
  • Gonads/cytology
  • Humans
  • Male
  • Ovarian Follicle/growth & development*
  • Polycystic Ovary Syndrome/etiology
  • Transforming Growth Factor beta/metabolism
  • Transforming Growth Factor beta/physiology*
  • Zebrafish Proteins/physiology*
(all 12)
PubMed
28856758 Full text @ Dev. Dyn.
Abstract
Aberrant signaling between germ cells and somatic cells can lead to reproductive disease and depends on diffusible signals, including TGFB-family proteins. The TGFB-family protein Gsdf (gonadal soma derived factor) controls sex determination in some fish and is a candidate for mediating germ cell/soma signaling.
Zebrafish expressed gsdf in somatic cells of bipotential gonads and expression continued in ovarian granulosa cells and testicular Sertoli cells. Homozygous gsdf knockout mutants delayed leaving the bipotential gonad state, but then became a male or a female. Mutant females ovulated a few oocytes, then became sterile, accumulating immature follicles. Female mutants stored excess lipid and down-regulated aromatase, gata4, insulin receptor, estrogen receptor, and genes for lipid metabolism, vitellogenin, and steroid biosynthesis. Mutant females contained less estrogen and more androgen than wild types. Mutant males were fertile. Genomic analysis suggests that Gsdf, Bmp15, and Gdf9, originated as paralogs in vertebrate genome duplication events.
In zebrafish, gsdf regulates ovarian follicle maturation and expression of genes for steroid biosynthesis, obesity, diabetes, and female fertility, leading to ovarian and extra-ovarian phenotypes that mimic human polycystic ovarian syndrome (PCOS), suggesting a role for a related TGFB signaling molecule in the etiology of PCOS. This article is protected by copyright. All rights reserved.
Genes / Markers
Figures
Figure Gallery (5 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b1279
    Indel
    b1280
      Small Deletion
      b1281
        Small Deletion
        1 - 3 of 3
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        Human Disease / Model
        Human Disease Fish Conditions Evidence
        polycystic ovary syndromeTAS
        1 - 1 of 1
        Show
        Sequence Targeting Reagents
        Target Reagent Reagent Type
        gsdfTALEN1-gsdfTALEN
        1 - 1 of 1
        Show
        Fish
        Antibodies
        Orthology
        Engineered Foreign Genes
        No data available
        Mapping