Honey bee aggression: evaluating causal links to disease-resistance traits and infection
Aggression is a context-dependent behavior that often represents an adaptive trade-off with other energetically demanding phenotypes. Diseases can impose strong selection pressures on an organism, impacting the expression of aggression if the behavior is physiologically or genetically linked to dise...
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Veröffentlicht in: | Behavioral ecology and sociobiology 2020-09, Vol.74 (9), p.1-14, Article 108 |
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Sprache: | eng |
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Zusammenfassung: | Aggression is a context-dependent behavior that often represents an adaptive trade-off with other energetically demanding phenotypes. Diseases can impose strong selection pressures on an organism, impacting the expression of aggression if the behavior is physiologically or genetically linked to disease resistance traits. However, aggression is also often a “sickness behavior” modulated directly by infection to conserve energy. Here we examine the cause-effect relationships between aggression and infection in the honey bee (Apis mellifera), a species with a heavy disease burden in which aggression has been correlated with diverse positive health outcomes. We induced infection in individual worker bees that differ in baseline aggression levels as a function of their colony-of-origin. We evaluated whether baseline aggression alters the response to infection, including the expression of disease-resistance behaviors and immune genes (defensin-1, hymenoptaecin, and vitellogenin). We found limited impact of baseline aggression on immune gene expression and the behavioral response to infection, but showed that infection can cause a change in aggression, at least in some cases. Though we cannot rule out the idea that high aggression is protective against infection, we find greater support for the idea that low aggression may be an energy-conserving “sickness behavior.” Future work concerning the evolutionary ecology of aggression and disease resistance in honey bees should consider the bidirectional relationship between these phenotypes, as well as the range of possible genetic and physiological mechanisms that connect them. |
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ISSN: | 0340-5443 1432-0762 |
DOI: | 10.1007/s00265-020-02887-0 |