A new study shows that mammalian species can "choose" the sex of their offspring in order to beat the odds and produce extra grandchildren. This chapter discusses the concept of sex reversal in mammals. The mammalian gonads are derived from the thickenings of the coelomic epithelium of. Sex, we are told, is pleasurable. Yet you probably wouldn't think that if you waded through the scientific literature. That's because most scientific.
It's August in Australia, and a small, mouse-like creature called an antechinus is busy killing himself through sex. He was a virgin until now, but. In mammals, primary sex determination is strictly chromosomal and is not usually influenced by the environment. The Y chromosome carries a gene that encodes a testis-determining factor. Unlike the situation in Drosophila (discussed below), the mammalian Y chromosome is a crucial. Sex, we are told, is pleasurable. Yet you probably wouldn't think that if you waded through the scientific literature. That's because most scientific.
The term sex steroids is nearly always synonymous with sex hormones (Wikipedia). Steroid hormones in mammals regulate diverse. How new species are created is at the core of the theory of evolution. Mammals may be a good example of how sex chromosome change drove. A new study shows that mammalian species can "choose" the sex of their offspring in order to beat the odds and produce extra grandchildren.
All rights reserved. He was a virgin until now, but for two to three weeks, this little lothario goes at it non-stop. He mates with as many females as he can, in violent, frenetic encounters that can each last up to 14 hours. He does little else. This burst of speed-mating is his one chance to pass his genes mammals to the next generation, and he will die trying. He exhausts himself so thoroughly that his body starts to fall apart.
His blood courses with testosterone and stress hormones. His fur falls off. He bleeds internally. His immune system fails to fight off incoming infections, and he becomes riddled with gangrene.
A few weeks shy of his first birthday, he is dead, along with every with male antechinus in the area. For semelparous animals, from salmon to mayflies, sex is a once-in-a-lifetime affair, and usually a fatal one. This sex is common among many animal groups, but rare among mammals. You only see it in the 12 species with antechinuses and a few close mamalsall of which are small, insect-eating marsupials. Sex they with like rodents and are colloquially called marsupial mice, antechinuses are more closely wiht to kangaroos and koalas than to mice or rats.
Why do these marsupials practice mammals reproduction, and why are they the only mammals that do so? The question has vexed biologists for three decades, mammals many have offered answers.
Yet others think the males are being altruistic, sacrificing themselves to leave more resources for sex next generation. Mammals Fisher, who has been studying antechinuses for decades, favours sex different idea. Her team gathered data on the lives and environments of a wide variety of with insect-eating marsupials, from the fully semelparous antechinuses, to relatives where a small number of males survive past their first sexual liaisons, to species that breed repeatedly.
These animals feed on insects, and some experience a glut of food once a year but very little at other times. This seasonality increases the further you get from the equator.
The species with mammala most seasonal menus also had shorter breeding seasons, and their males were more with to die after mating. Fisher thinks mammals as the ancestors of antechinuses spread south through Australia and New Guinea, they encountered strong yearly fluctuations in their sex supply.
Mammlas females were better at raising their young if they mammals birth just before the annual bonanza, and were with enough with wean their joeys. Their mating seasons shortened and synchronised, esx into a tight with of time. A baby shrew suckles for days or mammals a baby antechinus does so for mammals months. The females could only fit in one litter during the annual peak. Mammals had a huge impact on the males, which were forced to compete intensely with each other in a matter of weeks.
Rather than using claws or teeth, they competed with sperm. The more they had, the more females they impregnated, and with more likely they were to displace the sperm of maammals suitors.
Indeed, Fisher found a clear relationship between suicidal reproduction and testes size. The biggest testes of all, relative to body size, belong to species whose males die sex masse, followed by those where a minority survive to sex again, and then by those with several breeding seasons. The males that put the greatest efforts into sperm competition fathered the most young. These animals are short-lived anyway, so putting all their energy into one frenzied, fatal mating season was the best strategy for them.
Living fast and dying young was adaptive. She certainly finds it more plausible than the idea that the males are selflessly sex themselves for the next generation. Sperm competition drives the evolution of suicidal reproduction in mammals. Read Caption. Sex antechinus. By Ed Yong. Continue Reading.
Conversely, mothers in poor condition would likely play it safe, producing more daughters, whose productivity is physiologically limited. Other hypotheses make similar predictions -- that females who choose mates with particularly "good genes" e. The hypothesis was reinforced in in a seminal Nature paper by T. Clutton-Brock at the University of Cambridge, who found that among wild red deer, dominant mothers produced significantly more sons than deer who held a subordinate position within the herd.
Yet Garner and his colleagues were able to advance the research by reconstructing three-generation pedigrees of multiple species. They turned to the San Diego Zoo, enlisting the help of animal-care supervisor Greg Vicino in combing through decades of records on more than 38, animals from species. The project was labor-intensive, requiring years of work to reconstruct the pedigrees and breeding histories of the animals, Garner said. The researchers ended up with a pool of 1, granddams female grandparents and grandsires male grandparents for whom they had a complete record of three generations.
Major mammal groups were represented, including primates; carnivores, such as lions, bears and wolves; cloven-hoofed animals, such as cows, buffalo and deer; and odd-toed grazing animals, such as horses and rhinos. They found that when females produced mostly sons, those sons had 2. And the answer is yes," Garner said.
They're doing it for their own benefit. The same was true of grandsires, with the researchers showing that when grandfathers produced mostly sons, those sons on average had 2. But that could be entirely determined by the female," as she may be deciding the sex ratio to produce based on the quality of the male, Garner said. He compared the mating gambit to a kind of gambling game.
If I'm producing nothing but daughters, I'm making a safe bet -- I'm going to make the average. Sons, on the other hand, are a "high-risk, high-reward bet.
There may be 10 or 15 females but only one male that fathers everybody. The same is true with baboons. There is one alpha male. If you are the parent of that harem-holding male, then you have hit the genetic jackpot because he might produce tens or hundreds of offspring.
If you have a bachelor male, who never produces offspring, he produces zero. So males are a high-risk, high-payoff bet. Who would take the bet unless they knew they could rig it? A summary of the development of mammalian reproductive systems is shown in Figure Summary of the development of the gonads and their ducts in mammals. Several genes have been found whose function is necessary for normal sexual differentiation.
Unlike those that act in other developing organs, the genes involved in sex determination differ extensively between phyla, so one cannot look at Drosophila sex-determining genes and expect to see their homologues directing mammalian sex determination. However, since the phenotype of mutations in sex-determining genes is often sterility, clinical studies have been used to identify those genes that are active in determining whether humans become male or female.
Experimental manipulations to confirm the functions of these genes can be done in mice. In humans, the major gene for the testis-determining factor resides on the short arm of the Y chromosome. Individuals who are born with the short arm but not the long arm of the Y chromosome are male, while individuals born with the long arm of the Y chromosome but not the short arm are female. By analyzing the DNA of rare XX men and XY women, the position of the testis-determining gene has been narrowed down to a 35,base-pair region of the Y chromosome located near the tip of the short arm.
In this region, Sinclair and colleagues found a male-specific DNA sequence that could encode a peptide of amino acids. This peptide is probably a transcription factor, since it contains a DNA-binding domain called the HMG h igh- m obility g roup box.
This domain is found in several transcription factors and nonhistone chromatin proteins, and it induces bending in the region of DNA to which it binds Figure This gene is called SRY s ex-determining r egion of the Y chromosome , and there is extensive evidence that it is indeed the gene that encodes the human testis-determining factor.
It is thought that several testis-specific genes contain SRY-binding sites in their promoters or enhancers, and that the binding of SRY to these sites begins the developmental pathway to testis formation Cohen et al.
After Haqq et al. If SRY actually does encode the major testis-determining factor, one would expect that it would act in the genital ridge immediately before or during testis differentiation. This prediction has been met in studies of the homologous gene found in mice. The mouse gene Sry also correlates with the presence of testes; it is present in XX males and absent in XY females Gubbay et al.
The Sry gene is expressed in the somatic cells of the bipotential mouse gonad immediately before or during its differentiating into a testis; its expression then disappears Hacker et al.
The most impressive evidence for Sry being the gene for testis-determining factor comes from transgenic mice. Koopman and colleagues took the kilobase region of DNA that includes the Sry gene and presumably its regulatory elements and microinjected this sequence into the pronuclei of newly fertilized mouse zygotes.
In several instances, the XX embryos injected with this sequence developed testes, male accessory organs, and penises Figure Functional sperm were not formed, but they were not expected, either, because the presence of two X chromosomes prevents sperm formation in XXY mice and men, and the transgenic mice lacked the rest of the Y chromosome, which contains genes needed for spermatogenesis.
An XX mouse transgenic for Sry is male. A Polymerase chain reaction followed by electrophoresis shows the presence of the Sry gene in normal XY males and in a transgenic XX Sry mouse.
The gene is absent in a female XX littermate. B The external genitalia more When the Sry protein binds to its sites on DNA, it probably creates large conformational changes. It unwinds the double helix in its vicinity and bends the DNA as much as 80 degrees Pontiggia et al. This bending may bring distantly bound proteins of the transcription apparatus into close contact, enabling them to interact and influence transcription.
The identities of these proteins are not yet known, but they, too, are needed for testis determination. SRY may have more than one mode of action in converting the bipotential gonads into testes. It had been assumed for the past decade that SRY worked directly in the genital ridge to convert the epithelium into male-specific Sertoli cells. Recent studies Capel et al.
These mesonephric cells induce the gonadal epithelium to become Sertoli cells with male-specific gene expression patterns. The researchers found that when they cultured XX gonads with either XX or XY mesonephrons, the mesonephric cells did not enter the gonads. There was a strict correlation between the presence of Sry in the gonadal cells, mesonephric cell migration, and the formation of testis cords. Tilmann and Capel showed that mesonephric cells are critical for testis cord formation and that the migrating mesonephric cells can induce XX gonadal cells to form testis cords.
It appears, then, that Sry may function indirectly to create testes by inducing mesonephric cell migration into the gonad. In the experiment diagrammed, urogenital ridges containing both the mesonephric kidneys and gonadal rudiments were collected from day embryonic mice. One of the mice was marked with more The mapping of the testis-determining factor to the SRY region took scientists more than 50 years to accomplish. Moreover, other testis-forming genes have been found on the autosomes.
One of the autosomal genes involved in sex determination is SOX9 , which encodes a putative transcription factor that also contains an HMG box. Individuals having only one functional copy of this gene have a syndrome called campomelic dysplasia, a disease involving numerous skeletal and organ systems.
It appears that SOX9 is essential for testis formation. The mouse homologue of this gene, Sox9, is expressed only in male XY but not in female XX genital ridges. Moreover, Sox9 expression is seen in the same genital ridge cells as Sry, and it is expressed just slightly after Sry expression Wright et al. The Sox9 protein binds to a promoter site on the Amh gene, providing a critical link in the pathway toward a male phenotype Figure Synergism of Sox9 and Sf1 to activate the expression of the Amh gene.
A The binding of Sox9 to the Amh promoter initiates transcription of the Amh gene in the Sertoli cells. While Sry is found specifically in mammals, Sox9 is found throughout the vertebrates.
Sox9 may be the older and more central sex determination gene, although in mammals it became activated by its relative, Sry. Another protein that may be directly or indirectly activated by SRY is the transcription factor SF1 s teroidogenic f actor 1. Sf1 is necessary to make the bipotential gonad; but while Sf1 levels decline in the genital ridge of XX mouse embryos, the Sf1 gene stays on in the developing testis.
Sf1 appears to be active in masculinizing both the Leydig and the Sertoli cells. In the Leydig cells, Sf1 activates the genes encoding the enzymes that make testosterone. In , Bernstein and her colleagues reported two sisters who were genetically XY. Their Y chromosomes were normal, but they had a duplication of a small portion of the short arm of the X chromosome. Subsequent cases were found, and it was concluded that if there were two copies of this region on the active X chromosome, the SRY signal would be reversed Figure Bardoni and her colleagues proposed that this region contains a gene for a protein that competes with the SRY factor and that is important in directing the development of the ovary.
In testicular development, this gene would be suppressed, but having two active copies of the gene would override this suppression. This gene, DAX1 , has been cloned and shown to encode a member of the nuclear hormone receptor family Muscatelli et al. Dax1 is expressed in the genital ridges of the mouse embryo, shortly after Sry expression. Indeed, in XY mice, Sry and Dax1 are expressed in the same cells.
Thus, DAX1 is probably a gene that is involved in ovary determination. Phenotypic sex reversal in humans having two copies of the DAX1 locus. Two active more The WNT4 gene is another gene that may be critical in ovary determination.
This gene is expressed in the mouse genital ridge while it is still in its bipotential stage. Wnt4 expression then becomes undetectable in XY gonads which become testes , whereas it is maintained in XX gonads as they begin to form ovaries. In transgenic XX mice that lack the Wnt4 genes, the ovary fails to form properly, and its cells express testis-specific markers, including AMH- and testosterone-producing enzymes Vainio et al.
Sry may form testes by repressing Wnt4 expression in the genital ridge, as well as by promoting Sf1. One possible model is shown in Figure Possible mechanism for primary sex determination in mammals. While we do not know the specific interactions involved, this model attempts to organize the data into a coherent sequence.
Other models are possible. It should be realized that both testis and ovary development are active processes. Although remarkable progress has been made in recent years, we still do not know what the testis- or ovary-determining genes are doing, and the problem of primary sex determination remains as it has since prehistory one of the great unsolved problems of biology.
This had a huge impact on the males, which were forced to compete intensely with each other in a matter of weeks.
Rather than using claws or teeth, they competed with sperm. The more they had, the more females they impregnated, and the more likely they were to displace the sperm of earlier suitors.
Indeed, Fisher found a clear relationship between suicidal reproduction and testes size. The biggest testes of all, relative to body size, belong to species whose males die en masse, followed by those where a minority survive to mate again, and then by those with several breeding seasons.
The males that put the greatest efforts into sperm competition fathered the most young. These animals are short-lived anyway, so putting all their energy into one frenzied, fatal mating season was the best strategy for them. Living fast and dying young was adaptive. She certainly finds it more plausible than the idea that the males are selflessly sacrificing themselves for the next generation.
Sperm competition drives the evolution of suicidal reproduction in mammals. Read Caption. Brown antechinus. By Ed Yong. Continue Reading.