Genetic dissection of stress-induced reproductive arrest in Drosophila melanogaster females

PLoS Genet. 2018 Jun 11;14(6):e1007434. doi: 10.1371/journal.pgen.1007434. eCollection 2018 Jun.


By genetic manipulations, we study the roles played by insulin-producing cells (IPCs) in the brain and their target, the corpora allata (CA), for reproductive dormancy in female Drosophila melanogaster, which is induced by exposing them to a combination of low temperature (11°C), short-day photoperiod (10L:14D) and starvation (water only) for 7 days immediately after eclosion (dormancy-inducing conditions). Artificial inactivation of IPCs promotes, whereas artificial activation impedes, the induction of reproductive dormancy. A transcriptional reporter assay reveals that the IPC activity is reduced when the female flies are exposed to dormancy-inducing conditions. The photoperiod sensitivity of reproductive dormancy is lost in pigment-dispersing factor (pdf), but not cry, mutants, suggesting that light input to IPCs is mediated by pdf-expressing neurons. Genetic manipulations to upregulate and downregulate insulin signaling in the CA, a pair of endocrine organs that synthesize the juvenile hormone (JH), decrease and increase the incidence of reproductive dormancy, respectively. These results demonstrate that the IPC-CA axis constitutes a key regulatory pathway for reproductive dormancy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / cytology
  • Brain / metabolism
  • Corpora Allata / metabolism*
  • Down-Regulation
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / physiology*
  • Female
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Secreting Cells / metabolism
  • Juvenile Hormones / biosynthesis*
  • Juvenile Hormones / genetics
  • Reproduction / genetics*
  • Signal Transduction / genetics
  • Stress, Physiological / genetics*
  • Up-Regulation


  • Drosophila Proteins
  • Insulin
  • Juvenile Hormones

Grant support

This work was supported, in part, by Grants-in-Aid for Scientific Research from Ministry of Education, Culture, Sports, Science and Technology ( to DY (Nos. 16H06371, 16H02452, 017H05935 and 17K19371), to YH (No. 17K15155) and to HI (No. 16K06985), and a Shimonaka Memorial Foundation Grant ( to NO. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.