Temperature sensitivity of sexual differentiation of gonads in the European pond turtle: Hormonal involvement

✍ Scribed by Pieau, Claude ;Girondot, Marc ;Richard-Mercier, Noëlle ;Desvages, Gisèle ;Dorizzi, Mireille ;Zaborski, Patrick

• Publisher: John Wiley and Sons
• Year: 1994
• Tongue: English
• Weight: 936 KB
• Volume: 270
• Category: Article
• ISSN: 0022-104X
• DOI: 10.1002/jez.1402700110

✦ Synopsis

Abstract

In the European pond turtle, the incubation of eggs below 28°C yields 100% phenotypic males, whereas above 29.5°C 100% phenotypic females are obtained. Many data argue in favor of the involvement of steroid hormones in this phenomenon. During the thermosensitive period for sex determination, gonads are able to metabolize different steroid precursors, such as pregnenolone, progesterone, androstenedione, and dehydroepiandrosterone. Gonadal œstrogen content is higher at 30°C than at 25°C. When œstradiol benzoate (5 to 50 μg) or œstrone (100 μg) are injected into eggs incubated at 25°C before or at the beginning of the thermosensitive period, gonads differentiate into ovaries instead of testes: an ovarian‐cortex develops whereas medullary testicular cords are inhibited. Conversely, when tamoxifen (an antiœstrogen) is injected into eggs incubated at 30°C, medullary testicular cords (or tubes) differentiate. Gonadal aromatase activity during the thermosensitive period increases in an exponential fashion at 30°C, and remains very low at 25°C. When eggs are first incubated at 25°C up to a stage within this period, and then shifted to 35°C (a highly feminizing temperature) for different times, the response is also exponential, showing an amplification of aromatase synthesis. Temperature could act, directly or indirectly, on the regulation of the expression of the aromatase gene. The anti‐üullerian hormone (AMH) exerts an inhibitory effect on aromatase activity. The termination of the thermosensitive period could result in testes from an active synthesis of AMH, and in ovaries from high levels of œstrogens. © 1994 Wiley‐Liss, Inc.