Abstract
In many species including humans, aging reduces female fertility. Intriguingly, some animals preserve fertility longer under specific environmental conditions. For example, at low temperature and short day-length, Drosophila melanogaster enters a state called adult reproductive diapause. As in other stressful conditions, ovarian development arrests at the yolk uptake checkpoint; however, mechanisms underlying fertility preservation and post-diapause recovery are largely unknown. Here, we report that diapause causes more complete arrest than other stresses yet preserves greater recovery potential. During dormancy, germline stem cells (GSCs) incur DNA damage, activate p53 and Chk2, and divide less. Despite reduced niche signaling, germline precursor cells do not differentiate. GSCs adopt an atypical, suspended state connected to their daughters. Post-diapause recovery of niche signaling and resumption of division contribute to restoring GSCs. Mimicking one feature of quiescence, reduced juvenile hormone production, enhanced GSC longevity in non-diapausing flies. Thus, diapause mechanisms provide approaches to GSC longevity enhancement.
Highlights
In many species including humans, aging reduces female fertility
Our results suggest that diapause arrest slows germline progenitor senescence and facilitates post diapause recovery, raising the possibility that mimicking the diapause state in flies maintained in optimal growth conditions might be sufficient to slow germline stem cells (GSCs)
The results of this study provide insight into the cellular and molecular mechanisms that drive diapause arrest of ovarian development and facilitate recovery
Summary
In many species including humans, aging reduces female fertility. Intriguingly, some animals preserve fertility longer under specific environmental conditions. At low temperature and short day-length, Drosophila melanogaster enters a state called adult reproductive diapause. Many organisms enter a state of dormancy in response to environmental cues, which allows survival and a return to reproduction when conditions improve These states include diapause, dauer, and hibernation, among others[3,4,5,6]. While global changes in endocrine signaling, metabolism, and gene expression during Drosophila adult reproductive diapause have been documented[9,11,15,23,24,25], mechanisms that preserve fertility and drive post-diapause recovery are largely unknown. We report the effects of adult reproductive diapause on Drosophila germline stem cells (GSCs) and provide insights into the cellular and molecular mechanisms that preserve female reproductive potential
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