Temperature-dependent sex determination (TSD) is a type of environmental sex determination in which the temperatures experienced during embryonic development determine the sex of the offspring.[1] It is most prevalent and common among amniote vertebrates that are classified under the reptile class,[2] but is also used among some birds, such as the Australian Brush-turkey. It differs from the chromosomal sex-determination systems common among vertebrates. It is a type of environmental sex determination (ESD); in other ESD systems, some factors such as population determine the sex of organisms (see Polyphenism).
The eggs are affected by the temperature at which they are incubated during the middle one-third of embryonic development.[3] This critical period of incubation is known as the thermosensitive period (TSP).[4] The specific time of sex-commitment is known due to several authors resolving histological chronology of sex differentiation in the gonads of turtles with TSD.[3]
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Within the mechanism, two distinct patterns have been discovered and named Pattern I and Pattern II, with Pattern I further divided into IA and IB. Pattern IA has a single transition zone, where eggs predominantly hatch males if incubated below this temperature zone, and predominantly hatch females if incubated above it. Pattern IB also has a single transition zone, but females are produced below it and males above it. Pattern II has two transition zones, with males dominating at intermediate temperatures and females dominating at both extremes.[5] Very near or at the pivotal temperature of sex determination, mixed sex ratios and, more rarely, intersex individuals are produced.[6]
In turtles with TSD, males are generally produced at lower incubation temperatures than females (TSD IA), with this change occurring over a range of temperatures as little as 1-2 °C.[6] At cooler temperatures ranging between 22.5 and 27 degrees Celsius mostly male turtles arise, and at warmer temperatures around 30 degrees Celsius only female turtles arise.[7] In lizards and crocodilians, this pattern is reversed (TSD IB).
It has been proposed that essentially all modes of TSD are actually type II and those that deviate from the expected female-male-female pattern are simply never exposed to extreme temperature ranges on either end.[8]
Synergism between temperature and hormones has also been identified in these systems. Administering estradiol at male-producing temperatures generates females that are physiologically identical to temperature-produced females.[9] The reverse experiment, males produced at female temperatures, only occurs when a nonaromatizable testosterone or an aromatase inhibitor is administered, indicating that the enzyme responsible for conversion of testosterone to estradiol, aromatase, plays a role in female development.[10]
Interestingly, hormones and temperature show signs of acting in the same pathway, in that less hormone is required to produce a sexual shift as the incubation conditions near the pivotal temperature. It has been proposed[11] that temperature acts on genes coding for such steroidogenic enzymes, and testing of homologous GSD pathways has provided a genic starting point.[12] Yet, the genetic sexual determination pathway in TSD turtles is poorly understood and the controlling mechanism for male or female commitment has not been identified.[13]
While sex hormones have been observed to be influenced by temperature, thus potentially altering sexual phenotypes, specific genes in the gonadal differentiation pathway display temperature influenced expression.[14] In some species such important sex-determining genes as DMRT1[8] and those involved in the Wnt signalling pathway [14] could potentially be implicated as genes which provide a mechanism (opening the door for selective forces) for the evolutionary development of TSD.
The adaptive significance of TSD is currently not well understood. One possible explanation that TSD is common in amniotes is phylogenetic inertia – TSD is the ancestral condition in this clade and is simply maintained in extant lineages because it is currently adaptively neutral or nearly so.[15] Indeed, recent phylogenetic comparative analyses imply a single origin for TSD in most amniotes around 300 million years, with several more recent independent origins of TSD in squamates [16] and turtles. [17] Consequently, the adaptive significance of TSD in all but the most recent origins of TSD may have been obscured by the passage of deep time, with TSD potentially being maintained in many amniote clades simply because it ‘works’ (i.e. has no overall fitness costs along the lines of the phylogenetic inertia explanation).
Other work centers on a 1977 theoretical model (the Charnov–Bull model),[18][19] predicted that selection should favour TSD over chromosome-based systems when "the developmental environment differentially influences male versus female fitness";[2] this theoretical model was empirically validated thirty years later[2] but the generality of this hypothesis in reptiles is questioned. This hypothesis is supported by the persistence of TSD in certain populations of N. ocellatus, where it is advantageous to have females early in the season. The warmth early in the season ensures female-biased broods that then have more time to grow and reach maturity and possibly reproduce before they experience their first winter, thereby increasing fitness of the individual.[1]
"Temperature sex determination could allow the mother to determine the sex of her offspring by varying the temperature of the nest in which her eggs are incubated. However there is no evidence thus far that sex ratio is manipulated by parental care" [20]