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Updated: May 26, 2026
07:46
Detection of DNA Double-Stranded Breaks in Mouse Oocytes
Published on: June 23, 2023
Oocyte destruction is activated during viral infection
Travis C Thomson1, Anette Schneemann, Joshua Johnson
1Department of Obstetrics, Gynecology, and Reproductive Sciences/Division of Reproductive Endocrinology and Infertility, Yale School of Medicine, New Haven, Connecticut, USA.
Genesis (New York, N.Y. : 2000)
|December 17, 2011
Summary
Viral infection causes a starvation-like state in fruit flies, significantly reducing egg production by disrupting oogenesis. This study reveals a novel host-virus interaction affecting fly populations.
Area of Science:
- Virology
- Developmental Biology
- Genetics
Background:
- Viral infections can induce physiological changes mimicking starvation.
- Starvation and TOR kinase inhibition impair oocyte production in Drosophila melanogaster.
- Viral infection's impact on oogenesis was previously uncharacterized.
Purpose of the Study:
- To investigate the hypothesis that viral infection compromises oogenesis in Drosophila.
- To elucidate the mechanisms underlying viral-induced oocyte destruction.
- To identify host factors involved in viral pathogenesis and oogenesis.
Main Methods:
- Wild-type fruit flies were infected with flock house virus (FHV).
- Survival, embryo production, and Akt/TOR signaling were monitored.
- Oogenesis was assessed in wild-type and mutant flies (discs large, merlin, chc, synaptotagmin).
Main Results:
- FHV infection caused a dose-dependent reduction in fecundity and Akt/TOR signaling.
- Mid-oogenesis egg chamber destruction was observed, with FHV protein detected in developing egg chambers.
- Oogenesis was partially rescued in discs large and merlin mutants, and fully rescued in chc mutants, but not synaptotagmin mutants.
Conclusions:
- Viral infection disrupts Drosophila oogenesis through a mechanism involving Akt/TOR signaling.
- Host-virus interaction mechanisms controlling fly survival and egg chamber survival are distinct.
- This study identifies novel genetic and signaling pathways in a host-virus interaction impacting fly populations.
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