Deciphering the consequences of yolk testosterone metabolism in birds Inactivation or modification of an active signal


Meeting Abstract

P1-123  Friday, Jan. 4 15:30 – 17:30  Deciphering the consequences of yolk testosterone metabolism in birds: Inactivation or modification of an active signal? CAMPBELL, NA*; BOWDEN, RM; CASTO, JM; PAITZ, RT; Illinois St U; Illinois St U; Illinois St U; Illinois St U nacamp2@ilstu.edu

Maternal steroids transferred to eggs produce variable phenotypic effects in offspring. One maternal steroid that has garnered interest is testosterone due to its ability to elicit permanent, organizational effects in the brain and other tissues; however, vertebrate embryos actively regulate their maternal steroid exposure through steroid metabolism. We previously showed that in European starling (Sturnus vulgaris) eggs, testosterone is metabolized to etiocholanolone early in development which leads us to ask: When does this testosterone metabolism begin? And is etiocholanolone capable of influencing early growth of the developing embryo and extraembryonic membranes? To address the first question, 20 eggs were injected with tritiated testosterone (3H-T) and incubated for 0, 4, 8, and 12 hours to track the movement of testosterone early in development. To address the second question, 130 eggs were injected with either high (2.0 ng/egg), medium (1.0 ng/egg), or low (0.5 ng/egg) doses of etiocholanolone and sampled on days 3 and 5 of development to quantify the mass of the embryo and extraembryonic membranes. The conversion of testosterone to etiocholanolone was observed after only 4 hours of development. However, etiocholanolone manipulation had no significant effect on the growth rate of the embryos or extraembryonic membranes. This finding suggests that the conversion of yolk testosterone to etiocholanolone may be an inactivation pathway that buffers the embryo from the effects of maternal steroids.

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