Meeting Abstract
When transferred to egg yolks during oogenesis, maternally derived testosterone can alter offspring phenotypes. However, avian embryos readily metabolize testosterone to etiocholanolone early in incubation. Thus, it remains unclear whether testosterone or etiocholanolone mediates the phenotypic effects of maternal yolk testosterone, or whether this metabolism serves to inactivate the maternal steroid signal. Previously, injection of artificially incubated European starling (Sturnus vulgaris) eggs with etiocholanolone resulted in no detectable changes in embryonic phenotype after five days of incubation; however, few phenotypic traits were readily assessed at that embryonic age. Here, we examine the effects of in ovo etiocholanolone treatment on starling nestling phenotypes throughout nestling development. On the day they were laid, eggs were marked, injected with 5 ng of etiocholanolone in sesame oil, oil alone, or left uninjected, and returned to nests to complete incubation. The fates of eggs and their resulting nestlings were followed through fledging. At five, ten, and fifteen days of age, structural growth was assessed, and blood was collected to assess hematological development, blood glucose, and corticosterone titers. Pre- and post-hatching nesting success was similar among treatments. Structural growth and hematological development were also largely unaffected by experimental treatment. While it remains to be determined whether plasma concentrations of the metabolic hormone corticosterone were affected by treatment, preliminary analyses support the idea that embryonic metabolism of testosterone to eticholanolone serves to inactivate a maternal signal that influences offspring development rather than mediate the maternal effects of that signal.
