Genetic and neural modularity underlie the evolution of schooling behavior in threespine sticklebacks

Curr Biol. 2013 Oct 7;23(19):1884-8. doi: 10.1016/j.cub.2013.07.058. Epub 2013 Sep 12.


Although descriptions of striking diversity in animal behavior are plentiful, little is known about the mechanisms by which behaviors change and evolve between groups. To fully understand behavioral evolution, it will be necessary to identify the genetic mechanisms that mediate behavioral change in a natural context. Genetic analysis of behavior can also reveal associations between behavior and morphological or neural phenotypes, providing insight into the proximate mechanisms that control behavior. Relatively few studies to date have successfully identified genes or genomic regions that contribute to behavioral variation among natural populations or species, particularly in vertebrates. Here, we apply genetic approaches to dissect a complex social behavior that has long fascinated biologists, schooling behavior. We performed quantitative trait locus (QTL) analysis of schooling in an F2 intercross between strongly schooling marine and weakly schooling benthic sticklebacks (Gasterosteus aculeatus) and found that distinct genetic modules control different aspects of schooling behavior. Two key components of the behavior, tendency to school and body position when schooling, are uncorrelated in hybrids and map to different genomic regions. Our results further point to a genetic link between one behavioral component, schooling position, and variation in the neurosensory lateral line.

Publication types

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

MeSH terms

  • Animals
  • Behavior, Animal*
  • Biological Evolution*
  • Chromosome Mapping
  • Ectodysplasins / genetics
  • Lateral Line System / physiology
  • Models, Animal
  • Orientation / physiology
  • Quantitative Trait Loci / genetics*
  • Smegmamorpha / genetics*
  • Smegmamorpha / physiology
  • Social Behavior*
  • Vision, Ocular


  • Ectodysplasins