1. Developmental Biology
  2. Stem Cells and Regenerative Medicine
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JNK signaling triggers spermatogonial dedifferentiation during chronic stress to maintain the germline stem cell pool in the Drosophila testis

  1. Salvador C Herrera
  2. Erika A Bach  Is a corresponding author
  1. New York University School of Medicine, United States
Research Article
  • Cited 20
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Cite this article as: eLife 2018;7:e36095 doi: 10.7554/eLife.36095

Abstract

Exhaustion of stem cells is a hallmark of aging. In the Drosophila testis, dedifferentiated germline stem cells (GSCs) derived from spermatogonia increases during lifespan, leading to the model that dedifferentiation counteracts the decline of GSCs in aged males. To test this, we blocked dedifferentiation by mis-expressing the differentiation factor bag of marbles (bam) in spermatogonia while lineage-labeling these cells. Strikingly, blocking bam-lineage dedifferentiation under normal conditions in virgin males has no impact on the GSC pool. However, in mated males or challenging conditions, inhibiting bam-lineage dedifferentiation markedly reduced the number of GSCs and their ability to proliferate and differentiate. We find that bam-lineage derived GSCs have significantly higher proliferation rates than sibling GSCs in the same testis. We determined that Jun N-terminal kinase (JNK) activity is autonomously required for bam-lineage dedifferentiation. Overall, we show that dedifferentiation provides a mechanism to maintain the germline and ensure fertility under chronically stressful conditions.

Data availability

All data generated or analyzed during this study are included in the manuscript and supporting files. Source data files have been provided for Supplementary Files 1-3.

Article and author information

Author details

  1. Salvador C Herrera

    Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Erika A Bach

    Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, United States
    For correspondence
    bache02@nyu.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-5997-4489

Funding

National Institute of General Medical Sciences (R01 GM085075)

  • Erika A Bach

European Molecular Biology Organization

  • Salvador C Herrera

Human Frontier Science Program (LT000529-2015)

  • Salvador C Herrera

New York State Department of Health (NYSTEM N11G-292)

  • Erika A Bach

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Yukiko M Yamashita, University of Michigan, United States

Publication history

  1. Received: February 20, 2018
  2. Accepted: July 6, 2018
  3. Accepted Manuscript published: July 9, 2018 (version 1)
  4. Version of Record published: August 1, 2018 (version 2)

Copyright

© 2018, Herrera & Bach

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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