Mechanisms of TSD

There are several hypotheses concerning the physiological control of sex determination by temperature, but as of yet there is little conclusive evidence in support of a concrete molecular process (Standora and Spotila, 1985). What is known is that for all species with TSD, the ambient temperature during the middle third of incubation is critical in determining the sex ratio of the offspring (Janzen, 1991).

Among the possible mechanisms suggested are the influence of the H-Y antigen in the gonad, sex reversal in either males or females under the influence of temperature, and the temperature-influenced control of sex-determining DNA sequences (Standora and Spotila, 1985). The H-Y antigen hypothesis was one of the earlier possible molecular mechanisms proposed for TSD. The H-Y antigen was initially believed to be the testis-determining after it was detected in the heterogametic sex of a number of heterogametic animals, most of them homeotherms. However, subsequent studies have found inconsistencies among species with TSD when tested for TSD, and on a larger scale, H-Y antigen has been ruled out as the testis-determining factor for mammals (Janzen, 1991).More recently, researchers have focused on the role of steroids in gonadal differentiation, and in particular, the roles of estrogens and aromatase (Pieau et al, 1995).

Steroid hormones have been investigated as a potential mechanism for TSD with greater success. In particular, the enzyme aromatase has been fingered as a critical factor in the conversion of androgens such as testosterone into estrogens (Janzen, 1991; Pieau et al, 1995). When estrogens are placed onto the eggshell or injected into the eggs of species with TSD almost complete feminization of the embryos occurred, even at typically male producing temperatures (Janzen 1991; Pieau et al, 1995). Similarly, the application of aromatase inhibitors to eggs of Emys orbicularis resulted in masculinization of embryos (Pieau et al, 1991). The level of estrogen directly affects differentiation of the gonads in species with TSD with high levels leading to ovarian development and low levels associated with testicular cord development; androgens are believed to play a less critical role (Pieau et al, 1995). For this theory to be correct, there must be a mechanism for the thermosensitive regulation of transcription of the aromatase gene. The most likely method for this is that temperature affects the transcription of the aromatase gene through another factor such as cyclic AMP (Pieau et al, 1995).

Figure 3

Figure 3 depicts a possible molecular mechanism for TSD at female producing temperatures. Figure 3 adapted from Pieau, C., M. Girondot, G. Desvages, M. Dorizzi, N. Richard-Mercier, and P. Zaborski.“Temperature Variation and Sex Determination in Reptilia. Experimental Medecine 13 (1995): 516-523. Ecologie Systematique Evolution. 19 Sept. 2004 <http://www.ese.upsud.fr/epc/conservation/Publi/texte/BD_EM95.html>.

FT= female producing temperature

AMH= anti-Mullerian hormone

A= androstenedione

E1= estrone

E2= estradiol-17B

ER= estrogen receptor

T= testosterone

DHT= dihydrotestorsterone

hsp= heat-shock protein

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