Sex-determining mechanisms appear to change in response to environmental changes and/or intragenomic degeneration. For example, extant pelagic amniotes such as sea snakes and cetaceans universally exhibit viviparity as well as GSD, and fossil evidence demonstrates viviparity in several extinct marine reptiles [
Caldwell and Lee, 2001]. For these reasons, extinct marine reptiles like ichthyosaurs, mosasaurs, and sauropterygians most likely also exhibited GSD [
Organ et al., 2009]. Temperature-dependent sex determination would likely have precluded the ability of these species to be viviparous as maternal body temperatures, especially in deep ocean environments, would be too constant to incubate both male and female offspring in response to temperature. Extant marine reptiles such as sea turtles are not obligatorily pelagic. Their body plan allows them to exit the water and deposit gas-exchanging eggs on nesting beaches. However, the body plan of mosasaurs and other extinct pelagic reptiles did not permit transport of eggs to nesting beaches and amniotic eggs would not effectively exchange gases underwater. Therefore, we have hypothesized that GSD enabled viviparity and viviparity, in turn, facilitated adaptive radiation of pelagic amniotes [
Organ et al., 2009].
In addition to changes in habitat such as the transition from land to water, there are also environmental shifts in which local population sex ratios and resource availability could cause changes in intersexual differences in fitness. According to the Charnov-Bull hypothesis, TSD could allow parents finer control over offspring sex ratios in environments where intersexual differences in fitness make TSD adaptive [
Charnov and Bull, 1977]. Empirical support for this model was provided by
Warner and Shine [2008] in the form of enhanced fitness of males incubated at the natural temperature most likely to yield male offspring over fitness of males produced at other temperatures in jacky dragons,
Amphibolurus muricatus, a TSD lizard. The same pattern was reported for females incubated at the optimal female-producing temperature and females incubated at other temperatures. These studies suggest that SDMs change in response to environmental variation.
Intragenomic changes that may influence SDM involve the origin and degeneration of sex chromosomes. Sexually antagonistic genes are genes that are beneficial to one sex but detrimental to the other sex [
Arnqvist and Rowe, 2005]. The adaptive significance of sex chromosomes appears to be that they allow the sequestration of sexually antagonistic loci so that they are passed from parents either only to sons or daughters, depending on which sex carries the sex-specific chromosome [
Charlesworth et al., 2005]. Once sequestered on a nascent sex chromosome, sexually antagonistic genes can arise through the inhibition of recombination. Hemizygous regions – regions present in only one copy in the heterogametic sex – by necessity lack recombination. Such regions can arise by exaptation of a previously existing gene to a novel and sexually antagonistic function or by translocation of a sexually antagonistic locus to a nascent sex chromosome [
Graves, 2001]. The cessation of recombination that comes with hemizygosity leads to the accumulation of deleterious mutations in the absence of gene conversion or copy correction [
Rice, 1987;
Skaletsky et al., 2003;
Graves, 2006] ultimately resulting in a deleterious mutation load that leads to the dissolution of a sex chromosome. This conclusion has been invoked to explain the absence of a Y chromosome in the mole vole,
Ellobius lutescens, and other mammals [
Just et al., 1995]. It is possible that the demise of a sex chromosome due to purged excess of deleterious mutations leads to the loss of GSD and an opportunity for SDM shift [
Graves, 2006;
Mank and Avise, 2009].
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Determining Mechanisms Change Over Time
