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Déterminisme Sexuel

boy or a girl?

two fundamental types may be distinguished; asexual reproduction, in which a single organism separates into two or more equal or unequal parts; and sexual reproduction, in which a pair of specialized reproductive (sex) cells fuse.
Sexual reproduction occurs in many one-celled organisms and in all multicellular plants and animals. In higher invertebrates and in all vertebrates it is the exclusive form of reproduction, except in the few cases in which parthenogenesis is also possible. Sexual reproduction is essentially cellular in nature, i.e., it involves the fertilization of one sex cell (gamete) by another, producing a new cell (called a zygote), which develops into a new organism. The union of two isogametes (structurally identical but differing physiologically) is called isogamy, or conjugation, and occurs only in some lower forms (e.g., Spirogyra and some protozoa). Heterogamy is the fusion of two clearly differing kinds of gametes, distinguished as the ovum and the sperm .

    Multicellular plants alternate sexually reproducing, or gametophyte , and asexually reproducing, or sporophyte, generations. The gametophyte produces gametes, and the union of gametes results in the growth of a sporophyte; the sporophyte produces spores that give rise to a gametophyte. The prominent generation in lower plants (e.g., mosses, liverworts) and the complex fungi is the gametophyte; in the vascular plants (ferns, conifers, grasses, and flowering plants) it is the sporophyte. The less prominent generation may be an independent plant, as is the small inconspicuous gametophyte of ferns, or a reduced organism consisting of only a few cells and dependent for survival on the prominent form, like the pollen grain, which is the male gametophyte of seed plants.

    Many organisms exhibit special reproductive mechanisms to ensure fertilization; among higher plants the process of pollination may involve extremely complex interaction between the flower and the pollen-bearing agent (e.g., the yucca plant and the yucca moth). Among land-dwelling animals internal fertilization (copulation) is necessary in order to provide the fluid environment essential to fertilization.

    Sexual reproduction is of great significance in that, because of the fusion of two separate parental nuclei, the offspring inherit endlessly varied combinations of characteristics that provide a vast testing ground for new variations that may not only improve the species but ensure its survival. This probably explains the predominance of sexual reproduction among higher forms. Even in those microorganisms that reproduce asexually (e.g., bacteria) exchanges of hereditary material take place; in the hermaphroditic plants and animals (e.g., the earthworm) self-fertilization is almost always prevented by anatomical specializations or by differing maturation times for male and female gametes.
parthenogenesis :a form of reproduction in which the ovum develops into a new individual without fertilization. Natural parthenogenesis has been observed in many lower animals (it is characteristic of the rotifers), especially insects, e.g., the aphid . In many social insects, such as the honeybee and the ant, the unfertilized eggs give rise to the male drones and the fertilized eggs to the female workers and queens. The phenomenon of parthenogenesis was discovered in the 18th cent. by Charles Bonnet. In 1900, Jacques Loeb accomplished the first clear case of artificial parthenogenesis when he pricked unfertilized frog eggs with a needle and found that in some cases normal embryonic development ensued. Artificial parthenogenesis has since been achieved in almost all major groups of animals, although it usually results in incomplete and abnormal development. Numerous mechanical and chemical agents have been used to stimulate unfertilized eggs. In 1936, Gregory Pincus induced parthenogenesis in mammalian (rabbit) eggs by temperature change and chemical agents. No successful experiments with human parthenogenesis have been reported. The phenomenon is rarer among plants (where it is called parthenocarpy) than among animals. Unusual patterns of heredity can occur in parthenogenetic organisms. For example, offspring produced by some types are identical in all inherited respects to the mother.

Date: Mon Mar 23 14:07:48 1998
Posted By: Louise Freeman, Post-doc/Fellow Biology
Area of science: Genetics
ID: 886501218.Ge
Message:

Actually, most of what we think of as sexual characteristics are determined by a single gene, which is carried on the Y chromosome. This is the testis determination factor (TDF). Males get a copy of this gene; females do not. This gene acts during fetal development. Both XX and XY fetuses start out with the same sort of gonads. In males, the TDF causes the embryotic gonads to become testes. Without the TDF gene, the gonads become ovaries in female mammals.

Hormones produced by the developing testes determine what phenotypic sex the individual becomes. Both male and female fetuses have 2 sets of precursors to the adult genitalia: Mullerian ducts, which would develop into the uterus and fallopian tubes, and Wolfian, which would become the seminal vesicles and vas deferens. The fetal testes produce a hormone called Mullerian regression factor (MRF), which causes the Mullerian ducts to regress, or disappear. Thus, males do not develop a uterus. In females, who produce no MRF, the Mullerian ducts continue to grow, eventually becoming the female internal reproductive structures.

The other major hormone produced by the testes during development is the steroid hormone testosterone. Human males experience a surge of testosterone about midway through gestation; no such surge occurs in females. In some other mammals, like rats, the surge occurs late in gestation and continues for a week or so after birth. This testosterone has a variety of effects and influences not only the body but the behavior of animals.

One effect is to cause the Wolfian ducts to develop into the male reproductive tissues. Without testosterone, these structures regress in females, which is why females don't have seminal vesicles. In addition, the testosterone causes the development of the external male genitals: the penis. In the absence of testosterone, females develop a vagina and clitoris.

For these reasons, some scientists distingish between three different types of sex:
1) genotypic sex: Males are XY, females XX
2) gonadal sex: Males have testes, females ovaries
3) phenotypic sex: Males have penis, scrotum, etc. females vagina, uterus etc.

In most cases, these three types of sex agree, but under some conditions (experimental and natural) anomalies occur. More on this below.Sex can also be defined as hormonal (whether the individual has high levels of testosterone or estrogen) or behavioral (does it act more like a male or a female?)

After the developmental surge of testosterone, hormone levels fall and remain low throughout much of childhood, until they rise again with puberty and cause the development of male secondary sexual characteristics such as facial hair. However, experiments with animals show us that the early testosterone surge influences later behavior.

In rats, if you stop the action of developmental testosterone by removing the testes or treating the young males with anti-androgen drugs, you can change the appearance of the genitals. A complete androgen block will result in an animal that looks entirely female on the outside. In addition, when that animal grows up, it will behave more like a female. For instance, it will be less aggressive and, if courted by a normal male rat, will show female-like sexual behavior.

Conversely, if you treat developing female rats with testosterone, you can cause her external genitalia to look more like a male's. Such treatment also masculinizes the female's behavior: she will fight off a male rat who attempts to mate with her, but if she meets another female rat who is in estrus (or "heat") she will attempt to mount her as a male rat would.

Interestingly, certain hormone treatments (depending on the exact steroid given and at what point in development) can masculinize the body but not the brain, and vice versa. So you can get a female-looking rat acting like a male, and a male-looking rat who acts female. But all of these type of manipulations can result in the phenotypic sex (physical or behavioral) being different from that determined by the genotype.

Such manipulations in human fetuses, of course, would be unethical. But some "experiments of nature" show us that these same sort of effects occur in humans. One example is androgen insensitivity syndrome or AIS. Testosterone acts in cells by binding to a partucular protein, called the androgen receptor. The gene for this receptor is on the X chromosome, so females have 2 copies, males one. In AIS there is a mutation in the gene, so that the androgen receptor is either defective or missing. An XY male can have this mutation on the X chromosome and wind up completely insensitive to testosterone. Thus, although the testes form and produce hormones, testosterone cannot have its effects, and the external genitalia develop as a females. Internally, there is no uterus or fallopian tubes, since Mullerian regression factor made them regress. Humans like this look and usually think of themselves as female, but are sterile. There are even people with this condition working as actresses and models! This is an example of a genotypic and gonadal male producing a female phenotype.

Another human condition is congenital adrenal hyperplasia or CAH. Here, because a a defect in a different gene, the adrenal glands produce abnormally high levels of testosterone. If an XX human has this condition, the genitals can be masculinized, sometimes to the point where the child is mistaken for a boy at birth. The degree of masculinization varies, but depending on how much it is (and sometimes, when the condition is discovered), the decision may be made to raise the individual as a male. In other cases, the masculinization is treated surgically, (size of penis reduced, and vagina created) and the child raised female. In any case, this is an example of a genotypic and gonadal female having at least a partial male phenotype.

Another interesting case occurs in a particular strain of mice. In these animals, the part of the Y chromosome carrying the TDF has broken off and become attached to an X. If an XX individual inherits this TDF-carrying chromosome, the testes will develop, and the phenotype will be male. So here you would have a genotypic female that is a male gonadally and phenotypically.

I hope this answers your question, and shows how one very important gene, the TDF, can have multiple effects. However, sex determination is also influenced by other genes, such as the gene for the androgen receptor, and the genes that cause CAH. As with most human traits, multiple genes act together to produce the final phenotype. It also matters how you define sexual phenotype. You can consider the physical condition, the gonadal condition, the hormonal condition or behavior as phenotypic traits.

If you are interested in knowing more about this topic, I recommend the books Eve's Rib, by Robert Poole or the first few chapters of Behavioral Endocrinology by Becker, Breedlove and Crews.

I am interested in the evolution and ecology of sex-determining systems in vertebrates. My research program ranges from studies of the ecological context to the genetic architecture that gave rise to and maintain alternative mechanisms of sex determination. I am trying to understand the underlying ecological, physiological, behavioral, and molecular forces responsible for the persistence of temperature-dependent sex determination (TSD) over time. I also study life history evolution, ecological and conservation genetics of reptilian taxa, particularly turtles.

Currently, my main research focus is on the differences between the molecular mechanisms of temperature-dependent versus genotypic sex determination (GSD) in an evolutionary ecological context. My aim is to test whether molecular network involved in gonadal sexual differentiation in GSD and TSD species is essentially the same, but that qualitative and/or quantitative differences in expression of a few key genes in TSD species results in sex determination by temperature of egg incubation, rather than by genotypic constitution. Alternatively, differences in the regulatory regions of otherwise common sex-determining genes could be critical. To address this question I am using comparative analyses of gene expression patterns in embryos of TSD and GSD species prior to and during the embryological stages of sex-determination and gonadal differentiation.

Visit my homepage at:
http://www.public.iastate.edu/~nvalenzu/