Histone methyltransferase G9a is a key regulator of the starvation-induced behaviors in Drosophila melanogaster

Sci Rep. 2017 Nov 7;7(1):14763. doi: 10.1038/s41598-017-15344-2.

Abstract

Organisms have developed behavioral strategies to defend themselves from starvation stress. Despite of their importance in nature, the underlying mechanisms have been poorly understood. Here, we show that Drosophila G9a (dG9a), one of the histone H3 Lys 9-specific histone methyltransferases, functions as a key regulator for the starvation-induced behaviors. RNA-sequencing analyses utilizing dG9a null mutant flies revealed that the expression of some genes relating to gustatory perception are regulated by dG9a under starvation conditions. Reverse transcription quantitative-PCR analyses showed that the expression of gustatory receptor genes for sensing sugar are up-regulated in starved dG9a null mutant. Consistent with this, proboscis extension reflex tests indicated that dG9a depletion increased the sensitivity to sucrose under starvation conditions. Furthermore, the locomotion activity was promoted in starved dG9a null mutant. We also found that dG9a depletion down-regulates the expression of insulin-like peptide genes that are required for the suppression of starvation-induced hyperactivity. Furthermore, refeeding of wild type flies after starvation conditions restores the hyperactivity and increased sensitivity to sucrose as well as dG9a expression level. These data suggest that dG9a functions as a key regulator for the decision of behavioral strategies under starvation conditions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal*
  • Drosophila melanogaster / genetics
  • Drosophila melanogaster / physiology*
  • Epigenesis, Genetic
  • Histone Methyltransferases / metabolism*
  • Insulin / metabolism
  • Mutation
  • Peptides / genetics
  • Peptides / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Starvation*
  • Stress, Physiological*

Substances

  • Insulin
  • Peptides
  • Histone Methyltransferases