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Nuclear lamina dysfunction triggers a germline stem cell checkpoint

Author

Listed:
  • Lacy J. Barton

    (University of Iowa
    NYU School of Medicine)

  • Tingting Duan

    (University of Iowa)

  • Wenfan Ke

    (University of Iowa
    University of Virginia)

  • Amy Luttinger

    (University of Iowa)

  • Kaylee E. Lovander

    (University of Iowa)

  • Alexey A. Soshnev

    (University of Iowa
    The Rockefeller University)

  • Pamela K. Geyer

    (University of Iowa)

Abstract

LEM domain (LEM-D) proteins are conserved components of the nuclear lamina (NL) that contribute to stem cell maintenance through poorly understood mechanisms. The Drosophila emerin homolog Otefin (Ote) is required for maintenance of germline stem cells (GSCs) and gametogenesis. Here, we show that ote mutants carry germ cell-specific changes in nuclear architecture that are linked to GSC loss. Strikingly, we found that both GSC death and gametogenesis are rescued by inactivation of the DNA damage response (DDR) kinases, ATR and Chk2. Whereas the germline checkpoint draws from components of the DDR pathway, genetic and cytological features of the GSC checkpoint differ from the canonical pathway. Instead, structural deformation of the NL correlates with checkpoint activation. Despite remarkably normal oogenesis, rescued oocytes do not support embryogenesis. Taken together, these data suggest that NL dysfunction caused by Otefin loss triggers a GSC-specific checkpoint that contributes to maintenance of gamete quality.

Suggested Citation

  • Lacy J. Barton & Tingting Duan & Wenfan Ke & Amy Luttinger & Kaylee E. Lovander & Alexey A. Soshnev & Pamela K. Geyer, 2018. "Nuclear lamina dysfunction triggers a germline stem cell checkpoint," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06277-z
    DOI: 10.1038/s41467-018-06277-z
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