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Deletion of inositol polyphosphate 4-phosphatase type-II B affects spermatogenesis in mice

Yasemin Ceyhan1, Manqi Zhang2, Jingtao Guo3,4

  • 1Department of Human and Molecular Genetics, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, United States of America.

Plos One
|May 16, 2020
PubMed

Insights

Inositol polyphosphate-4-phosphatase type II (INPP4B) deletion impairs male fertility in mice. INPP4B deficiency reduces sperm count and testicular function, particularly with aging and high-fat diets.

Area of Science:

  • Molecular Biology
  • Reproductive Biology
  • Oncology

Background:

  • Inositol polyphosphate-4-phosphatase type II (INPP4B) is a dual-specificity phosphatase with tumor suppressor roles.
  • INPP4B dephosphorylates specific phospholipids, inhibiting key signaling pathways like AKT and PKC.
  • High INPP4B expression in testes suggests a role in male reproductive physiology.

Purpose of the Study:

  • To investigate the impact of Inpp4b deletion on testicular function in a mouse model.
  • To determine if Inpp4b deficiency affects sperm production, germ cell differentiation, and testicular response to environmental factors.

Main Methods:

  • Generation and analysis of Inpp4b knockout (Inpp4b-/-) male mice.
  • Comparison of testicular size, sperm count, germ cell apoptosis, and gene/protein expression (steroidogenic enzymes, LH receptor, AR, γH2A.X) between Inpp4b-/- and wild-type (WT) mice.
  • Assessment of effects of aging and high-fat diet (HFD) on Inpp4b-/- male reproductive parameters.

Main Results:

  • Inpp4b-/- male mice exhibited significantly smaller testes and reduced mature sperm production compared to WT.
  • Germ cell apoptosis was elevated, and meiotic marker γH2A.X expression was decreased in Inpp4b-/- testes.
  • Inpp4b deficiency led to reduced expression of early steroidogenic enzymes and LH receptor, with no change in AR protein levels. The negative effects on sperm count were exacerbated by age and HFD.

Conclusions:

  • INPP4B is crucial for maintaining male germ cell differentiation and overall testicular function.
  • Inpp4b deletion compromises testicular function and exacerbates negative impacts of aging and high-fat diet on male fertility.
  • INPP4B may serve as a protective factor against age- and diet-related testicular dysfunction.

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