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Author Spotlight: Exploring Cellular Zinc Regulation Through ZnT1 Functionality
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Zinc Deficiency Disrupts Germ Cell Nest Breakdown During In Vitro Ovary Culture.

James M Hester1,2, Suzanne M Getman3, Melissa E Pepling3

  • 1Integrative and Biomedical Physiology Program, The Pennsylvania State University, University Park, Pennsylvania, USA.

Molecular Reproduction and Development
|February 12, 2026
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Zinc deficiency disrupts primordial follicle formation in newborn mice, reducing oocyte numbers and potentially impacting fertility. This essential mineral is crucial for early ovarian development and female reproductive health.

Keywords:
follicleovaryzinc

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Area of Science:

  • Reproductive Biology
  • Developmental Biology
  • Nutritional Science

Background:

  • Mammalian primordial follicles are vital for lifelong gamete supply.
  • The initial size of the primordial follicle pool dictates reproductive longevity.
  • Impaired follicle assembly severely compromises female fertility.

Purpose of the Study:

  • To investigate the impact of zinc deficiency on germ cell survival and follicle activation.
  • To assess zinc's role in primordial follicle formation and early postnatal ovarian development.
  • To analyze the effect of zinc deficiency on key regulatory gene expression during nest breakdown.

Main Methods:

  • In vitro organ culture of mouse ovaries during late pregnancy and early postnatal stages.
  • Assessment of apoptosis, germ cell number, and gene expression in fetal and newborn ovaries.
  • Evaluation of germ cell nest breakdown, primordial follicle formation, and follicle activation.

Main Results:

  • Zinc deficiency did not affect apoptosis, germ cell number, or gene expression in fetal ovaries.
  • Germ cell nest breakdown was disrupted by zinc deficiency, resulting in fewer oocytes within primordial follicles.
  • Zinc deficiency decreased the gene expression of oocyte-specific (Bmp15) and granulosa cell-specific (Foxl2) factors.
  • A trend towards fewer activated growing follicles was observed in zinc-deficient newborn ovaries.

Conclusions:

  • Zinc deficiency impairs primordial follicle formation by disrupting germ cell nest breakdown in newborn mice.
  • Reduced expression of Bmp15 and Foxl2 may underlie the observed defects in follicle assembly.
  • Disruption of early follicle activation and primordial follicle formation due to zinc deficiency may negatively impact subsequent fertility.