Kr-h1 maintains distinct caste-specific neurotranscriptomes in response to socially regulated hormones

Cell. 2021 Nov 11;184(23):5807-5823.e14. doi: 10.1016/j.cell.2021.10.006. Epub 2021 Nov 4.


Behavioral plasticity is key to animal survival. Harpegnathos saltator ants can switch between worker and queen-like status (gamergate) depending on the outcome of social conflicts, providing an opportunity to study how distinct behavioral states are achieved in adult brains. Using social and molecular manipulations in live ants and ant neuronal cultures, we show that ecdysone and juvenile hormone drive molecular and functional differences in the brains of workers and gamergates and direct the transcriptional repressor Kr-h1 to different target genes. Depletion of Kr-h1 in the brain caused de-repression of "socially inappropriate" genes: gamergate genes were upregulated in workers, whereas worker genes were upregulated in gamergates. At the phenotypic level, loss of Kr-h1 resulted in the emergence of worker-specific behaviors in gamergates and gamergate-specific traits in workers. We conclude that Kr-h1 is a transcription factor that maintains distinct brain states established in response to socially regulated hormones.

Keywords: ants; brain; gene regulation; plasticity; social behavior.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ants / drug effects
  • Ants / genetics*
  • Ants / physiology
  • Behavior, Animal / drug effects
  • Brain / metabolism
  • Ecdysterone / pharmacology*
  • Gene Expression Regulation / drug effects
  • Genome
  • Hierarchy, Social*
  • Insect Proteins / metabolism*
  • Neurons / drug effects
  • Neurons / metabolism*
  • Phenotype
  • Repressor Proteins / metabolism
  • Sesquiterpenes / pharmacology*
  • Signal Transduction / drug effects
  • Social Behavior*
  • Transcriptome / drug effects
  • Transcriptome / genetics*


  • Insect Proteins
  • Repressor Proteins
  • Sesquiterpenes
  • Ecdysterone
  • juvenile hormone III