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Updated: Mar 1, 2026

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Origin of a rapidly evolving homeostatic control system programming testis function.

Pengli Bu1,2, Shintaro Yagi3, Kunio Shiota3,4

  • 1Institute for Reproductive Health and Regenerative MedicineUniversity of Kansas Medical Center, Kansas City, Kansas, USA.

The Journal of Endocrinology
|June 4, 2017
PubMed
Summary
This summary is machine-generated.

Researchers discovered a new gene, Prl3c1, that controls testis growth and function in male mice. Deleting this gene caused larger testes and higher hormone levels, revealing a novel reproductive control system.

Keywords:
Leydig cellsprolactin familytestistransposable elements

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Area of Science:

  • Reproductive biology
  • Molecular endocrinology
  • Mammalian genetics

Background:

  • Mammals share reproductive regulation strategies via the hypothalamic-pituitary-gonadal axis.
  • Species-specific differences in reproductive performance exist despite conserved mechanisms.
  • The prolactin gene family member, Prl3c1, was initially identified as a uterine cytokine.

Purpose of the Study:

  • To investigate the role of Prl3c1 in the male reproductive axis.
  • To characterize the reproductive phenotype of Prl3c1-null mice.
  • To elucidate the mechanism of species-restricted homeostatic control of testicular function.

Main Methods:

  • Mouse mutagenesis to generate Prl3c1-null models.
  • Phenotypic analysis of male reproductive organs and hormone levels.
  • Transcriptional analysis (5'RACE), chromatin immunoprecipitation, and DNA methylation studies.
  • Comparative analysis of the Prl3c1 locus across five murid rodent species.

Main Results:

  • Prl3c1-null male mice exhibited testiculomegaly and hyperandrogenism.
  • Testicular enlargement was linked to an expanded Leydig cell compartment.
  • Two distinct Prl3c1 transcripts (Prl3c1-v1 and Prl3c1-v2) were identified with tissue-specific expression.
  • Prl3c1-v2, expressed in Leydig cells, encodes a protein (PLP-J V2) with Leydig cell-static actions.
  • The testicular transcript and protein result from a recent retrotransposition event.

Conclusions:

  • Prl3c1 acts as a species-restricted homeostatic regulator of testicular growth and function.
  • Alternative splicing and promoter usage generate distinct Prl3c1 protein isoforms with specific actions.
  • PLP-J V2 plays a critical role in controlling Leydig cell proliferation and function.
  • This study reveals a novel regulatory system impacting male reproductive setpoints.