The adaptive significance of temperature-dependent sex determination (TSD) has attracted a great deal of research, but the underlying mechanisms by which temperature determines the sex of a developing embryo remain poorly understood. Here, we manipulated the level of a thyroid hormone (TH), triiodothyronine (T
3
), during embryonic development (by adding excess T
3
to the eggs of the red-eared slider turtle
Trachemys scripta
, a reptile with TSD), to test two competing hypotheses on the proximate basis for TSD: the
developmental rate hypothesis
versus the
hormone hypothesis
. Exogenous TH accelerated embryonic heart rate (and hence metabolic rate), developmental rate, and rates of early post-hatching growth. More importantly, hyperthyroid conditions depressed expression of
Cyp19a1
(the gene encoding for aromatase) and levels of oestradiol, and induced more male offspring. This result is contrary to the direction of sex-ratio shift predicted by the
developmental rate hypothesis
, but consistent with that predicted by the
hormone hypothesis
. Our results suggest an important role for THs in regulating sex steroid hormones, and therefore, in affecting gonadal sex differentiation in TSD reptiles. Our study has implications for the conservation of TSD reptiles in the context of global change because environmental contaminants may disrupt the activity of THs, and thereby affect offspring sex in TSD reptiles.
Molecular players involved in temperature-dependent sex determination and sex differentiation in Teleost fish
