Meeting Abstract
Hormones are dynamic signaling molecules that influence both gene activity and behavioral phenotypes, and are thus thought to play a central role in phenotypic evolution. The steroid hormone testosterone (T), for example, mediates many life history and behavioral traits that influence fitness, and it is therefore hypothesized that changes in T or its regulation contribute to phenotypic evolution. The mechanisms by which T might bring about such evolutionary changes are unclear, however, in part because T is not a direct gene product but is instead synthesized via a multi-enzyme biosynthetic pathway, which is itself activated by a complex endocrine cascade. Here, we sought to identify mechanistic sources of variation in T production, by comparing two behaviorally divergent subspecies of dark-eyed junco (Junco hyemalis), in the wild and in captivity. In a series of experiments, we show that variation in (a) the gonad’s molecular capacity to produce T and (b) the timecourse over which T elevates following HPG axis stimulation explain more phenotypic variation than has been appreciated to date. Critically, our results point to specific genes in the gonadal steroidogenic pathway that fulfill key conditions for phenotypic evolution, i.e. they vary functionally in their expression among individuals and between populations, and they map onto population variation in T and T-mediated traits in a common garden. We also present findings on gonadal sensitivity to corticosterone and gonadotropin-inhibitory hormone, which may act directly on the gonad to suppress steroidogenesis. Our findings support the view that variation in endocrine signaling in tissues other than the brain may be a far more important contributor to phenotypic variation and evolution than previously thought.
