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A defect in the peroxisomal biogenesis in germ cells induces a spermatogenic arrest at the round spermatid stage in

Ann-Kristin Brauns1, Markus Heine2, Klaus Tödter2

  • 1Department of Anatomy and Experimental Morphology, University Medical Center Hamburg-Eppendorf (UKE), 20246, Hamburg, Germany. a.brauns@uke.de.

Scientific Reports
|July 4, 2019
PubMed

Insights

Peroxisome defects disrupt spermatogenesis in mice, causing abnormal lipid profiles and impaired sperm development. This study highlights peroxisomes' crucial role in male fertility.

Area of Science:

  • Cell Biology
  • Reproductive Biology
  • Biochemistry

Background:

  • Peroxisomes degrade very long-chain fatty acids (VLCFAs) and are essential for cellular metabolism.
  • Peroxisomal dysfunction is linked to neurological and testicular abnormalities, but specific testicular alterations remain unclear.
  • PEX13 is vital for peroxisome biogenesis, and its inactivation causes peroxisomal defects.

Purpose of the Study:

  • To investigate the role of peroxisomes in spermatogenesis using a germ cell-specific knockout of Pex13 in mice.
  • To characterize the testicular alterations resulting from impaired peroxisome function during male germ cell development.

Main Methods:

  • Generation of a germ cell-specific Pex13 knockout mouse model using STRA8-inducible Cre recombinase.
  • Analysis of testicular histology, lipid composition (gas chromatography), and gene expression in Pex13 knockout mice.
  • Assessment of the blood-testis barrier (BTB) integrity.

Main Results:

  • Pex13 knockout mice exhibited interrupted germ cell differentiation at the round spermatid stage, leading to multinucleated giant cells (MNCs) and loss of mature spermatids.
  • Significant alterations in testicular lipid composition, including increased shorter fatty acids and decreased docosahexaenoic acid (C22:6n-3) and docosapentaenoic acid (C22:5n-6).
  • Down-regulation of genes involved in metabolite transport and peroxisomal β-oxidation, alongside alterations in blood-testis barrier structural components.

Conclusions:

  • Germ cell-specific inactivation of Pex13 severely impairs spermatogenesis in mice.
  • Peroxisomal defects lead to significant metabolic and structural changes within the testes, affecting lipid metabolism and BTB integrity.
  • These findings underscore the critical role of peroxisomes in maintaining male reproductive function.

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