RT Journal Article
SR Electronic
T1 Transcriptomic support for the Immunocompetence Handicap Hypothesis but not the Oxidation Handicap Hypothesis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 814178
DO 10.1101/814178
A1 Daniel J. Newhouse
A1 Ben J. Vernasco
YR 2019
UL http://biorxiv.org/content/early/2019/10/22/814178.abstract
AB Sexually selected traits are hypothesized to be honest signals of individual quality due to the costs associated with their development or expression. Testosterone, a sex steroid known to influence the production of sexually selected traits, has been proposed to underlie the costs associated with sexually selected traits via its immunosuppressive effects (i.e., the Immunocompetence Handicap Hypothesis) or by influencing an individual’s exposure/susceptibility to oxidative stress (i.e., the Oxidation Handicap Hypothesis). Previous work testing these hypotheses has primarily focused on physiological measurements of immunity or oxidative stress, but little is known about the molecular pathways by which testosterone could influence immunity and/or oxidative stress pathways. To measure the molecular consequences of experimentally elevated testosterone, we used previously published RNA-seq data from studies that measured the transcriptome of individuals treated with either a testosterone-filled or an empty (i.e., control) implant. Two studies encompassing two species of bird and three tissue types fit our selection criteria. We found strong support for the Immunocompetence Handicap Hypothesis, but no support for the Oxidation Handicap Hypothesis. More specifically, testosterone-treated individuals exhibited strong signatures of immunosuppression, encompassing both cell-mediated and humoral immunity. Our results suggest that testosterone enforces the honesty of sexually-selected traits by influencing an individual’s immunocompetence rather than their exposure or susceptibility to oxidative stress.