Longevity PapersAbout
← All papers
RESEARCH PAPER / 2024-10-29

Germ cell progression through zebrafish spermatogenesis declines with age.

Andrea L Sposato, Hailey L Hollins, Darren R Llewellyn, Jenna M Weber, Madison N Schrock, Jeffrey A Farrell, James A Gagnon

School of Biological Sciences, University of Utah, Salt Lake City, UT 84112, USA.School of Biological Sciences, University of Utah, Salt Lake City, UT 84112, USA. · pubmed

Abstract

Vertebrate spermatogonial stem cells maintain sperm production over the lifetime of an animal, but fertility declines with age. Although morphological studies have informed our understanding of typical spermatogenesis, the molecular and cellular mechanisms underlying the maintenance and decline of spermatogenesis are not yet understood. We used single-cell RNA sequencing to generate a developmental atlas of the aging zebrafish testis. All testes contained spermatogonia, but we observed a progressive decline in spermatogenesis that correlated with age. Testes from some older males only contained spermatogonia and a reduced population of spermatocytes. Spermatogonia in older males were transcriptionally distinct from spermatogonia in testes capable of robust spermatogenesis. Immune cells including macrophages and lymphocytes drastically increased in abundance in testes that could not complete spermatogenesis. Our developmental atlas reveals the cellular changes as the testis ages and defines a molecular roadmap for the regulation of spermatogenesis.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the decline of spermatogenesis in aging zebrafish, which is relevant to understanding the biological mechanisms of aging and fertility. While it provides valuable insights into the cellular and molecular changes associated with aging in the testis, the findings are more descriptive and incremental rather than groundbreaking. The research contributes to the field by mapping changes in spermatogonial stem cells and immune cell dynamics, but it does not propose solutions or interventions that could directly address the root causes of aging.

Author of this paper? Send a correction.