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Reproduction is a fundamental process of life. All living organisms must reproduce either asexually (e.g., bacteria) or sexually (e.g., mammals). Asexual reproduction is highly efficient and produces large numbers of genetically identical offspring in a relative short amount of time. This strategy, however, is vulnerable to environmental changes because genetic and phenotypic variation between individual progeny is minimal and consequently the probability of producing progeny that have beneficial traits in a hostile environment is relatively low. In contrast, sexual reproduction is less efficient but produces progeny with markedly increased genetic and phenotypic variation, which increases the probability of producing individuals with characteristics that may be adaptive to environmental changes. In this context, natural selection favors sexual reproduction, and consequently most extant animals and flowering plants reproduce sexually.
In sexual reproduction a new individual is created by combining the genetic material of two individuals. Sexual reproduction involves the evolution of two sexually dissimilar individuals belonging to the same species, one male and one female, and each equipped with its own specific attributes necessary for its particular contribution to the process of procreation. Each sex produces its own type of sex cell or gamete, and the union of male and female gametes generates species-specific progeny. In addition, mechanisms—some simple, some complex—have evolved to ensure the proximity and union of the sex cells, known as syngamy. Thus, within each species, the relevant sexual characteristics of each partner have adapted differently to achieve the most efficient union of these progenitor cells. These differences between the sexes of one species are called sexual dimorphism. For example, oviparous species such as frogs release their eggs into a liquid medium only when they are in relative proximity to sperm. As effective as this approach is, it also typifies the wastefulness of reproduction among higher species inasmuch as most gametes go unfertilized.
Even among species that normally reproduce sexually, sexual dimorphism is not universal. For example, monoecious (i.e., hermaphroditic) species, such as cestodes and nematodes, have the capacity to produce both sperm and eggs. By definition, the ability to produce just one kind of gamete depends on sexually dimorphic differentiation.
Organisms that reproduce sexually normally have a single pair of sex chromosomes that are morphologically distinguishable from other chromosomes, the autosomes. Each of the sex chromosomes carries genetic information that determines the primary and secondary sexual characteristics of an individual; that is, whether the individual functions and appears as male or female. It has become abundantly clear that genes determine sexual differentiation and sexual expression and, as a result, mechanisms and patterns of reproduction.
The sex of the gonad is genetically programmed: Will a female gonad (ovary) or a male gonad (testis) develop? Although germ cells of the early embryonic gonad are totipotent, these cells develop into female gametes or ova if the gonad becomes an ovary, but they develop into male gametes or sperm if the gonad becomes a testis. These two anatomically and functionally distinct gonads determine either “maleness” or “femaleness” and dictate the development of both primary and secondary sexual characteristics. Endocrine and paracrine modulators that are specific for either the ovary or the testis are primarily responsible for female or male sexual differentiation and behavior and therefore the individual's role in procreation. N53-1
Gender —or, more accurately, gender identification—refers to the concept held by the individual (or by those raising the individual) that the individual is male, female, or ambivalent.
Sex refers to biological characteristics that distinguish female from male. The distinction may be made on the basis of chromosomes, gonads, internal and external morphology, and hormonal status.
Gametes derive from a specialized lineage of embryonic cells—the germline —known as germ cells. They are the only cells that can divide by mitosis and meiosis and differentiate into sperm or ova. Germ cells are therefore the critical link between generations. The process by which cells decide between becoming somatic cells of the body or germ cells occurs in the early embryo and involves factors and processes that prevent the somatic fate and induce germline differentiation. Studies in experimental model systems are beginning to unravel the complex process of germline determination, which involves germline-specific transcription factors (see pp. 81–88 ) and small noncoding RNAs (see pp. 99–100 ) and DNA methylation (see pp. 95–96 ) to control expression of specific genes. The process by which germ cells develop into either sperm or ova is referred to as gametogenesis and involves meiosis.
Except for the gametes, all other nucleated cells in the human body— somatic cells —have a diploid number (2N) of chromosomes. Human diploid cells have 22 autosome pairs consisting of two homologous chromosomes, one contributed by the father and one by the mother. Diploid cells also contain a single pair of sex chromosomes comprising either XX or XY. Each somatic cell in human females has 44 autosomes (i.e., 22 pairs) plus two X chromosomes, and each somatic cell in males has 44 autosomes plus one X and one Y chromosome. The karyotype is the total number of chromosomes and the sex chromosome combination, and thus in normal females is designated 46,XX, and in normal males, 46,XY ( Fig. 53-1 ). Gametes have a haploid number (N) of chromosomes and contain either an X or Y sex chromosome.
The representation in Figure 53-1 is obtained by taking photomicrographs of chromosomes and then rearranging them as shown. The chromosomes are numbered according to size, the largest chromosomes having the smallest number. Pairs of homologous chromosomes are identified on the basis of size, patterns of banding, and the placement of centromeres.
In the case of humans, one generally uses leukocytes (white blood cells) that have been treated with a hypotonic solution to cause swelling and thus help disperse the chromosomes, and with colchicine to arrest mitosis in metaphase. A dye is then applied to visualize the chromosomes better.
Mitosis is the only kind of cell division that occurs in somatic cells. Mitosis results in the formation of two identical daughter cells ( Fig. 53-2 A ), each having the same number of chromosomes (i.e., 46 in humans) and the same DNA content as the original cell. After interphase, during which nuclear DNA in the form of chromatin replicates, mitosis proceeds in a continuum of five phases:
Prophase. The replicated chromatin condenses into 46 chromosomes that comprise two identical sister chromatids bound together at the centromere.
Metaphase. The nuclear envelope breaks down, the chromosomes align along the midplane of the cell known as the metaphase plate, and microtubules enter the nuclear space and attach to the centromere of each chromosome.
Anaphase. The centromeres dissolve and the microtubules pull apart the sister chromatids toward opposite poles of the cell.
Telophase. A new nuclear membrane envelopes each cluster of chromatids, which decondense back into chromatin.
Cytokinesis. The cell divides into two genetically identical daughter cells, each containing one of the nuclei.
Figure 53-2 B in the text shows meiosis in the male, whereas Figure 53-2 C shows meiosis in the female.
In both males and females, the primordial germ cell (PGC) enters the gonad and undergoes many rounds of mitotic divisions. At some point, both a spermatogonium (in the case of males) and an oogonium (in the case of females) enter the first of two meiotic divisions (top cell in Fig. 53-2 B, C ).
In the case of males (see Fig. 53-2 B ), one primary spermatocyte (diploid 4N DNA)—a cell that has just entered prophase I—ultimately gives rise to two secondary spermatocytes (haploid 2N DNA) at the completion of the first meiotic division, and four spermatids (haploid 1N DNA) at the completion of the second meiotic division. Thus, one primary spermatocyte yields four mature gametes.
In the case of females (see Fig. 53-2 C ), one primary oocyte (diploid 4N DNA)—a cell that is arrested in prophase I until shortly before ovulation—ultimately gives rise to one secondary oocyte (haploid 2N DNA) and one diminutive first polar body (haploid 2N DNA) at the completion of the first meiotic division. The polar body is equivalent to one of the two cells at telophase I in Figure 53-2 B . In the second meiotic division, which the cell completes at the time of fertilization, the secondary oocyte gives rise to one mature oocyte (haploid 1N DNA) and a diminutive second polar body (haploid 1N DNA). Thus, unlike the situation in males, one primary oocyte yields one mature gamete—equivalent to one of the four cells at the bottom of Figure 53-2 B .
Note that the first polar body sometimes divides during meiosis II, thereby yielding a total of three polar bodies and one oocyte. This is the same amount of DNA produced in spermatogenesis (i.e., four spermatids from one spermatogonium).
Daughter cells produced by mitosis are genetically identical because there is no exchange of genetic material between homologous chromosomes and the sister chromatids of each chromosome split, one going to each daughter cell during anaphase of the single mitotic division.
Meiosis occurs only in germ cells— spermatogonia in males and oogonia in females—still with a complement of 2N DNA (N = 23). Germ cells initially multiply by mitosis and then enter meiosis when they begin to differentiate into sperm (see Fig. 53-2 B ) or ova (see Fig. 53-2 C ). Gametogenesis reduces the number of chromosomes by half, so that each gamete contains one chromosome from each of the original 23 pairs. This reduction in genetic material from the diploid (2N) to the haploid (N) number involves two divisions referred to as meiosis I and meiosis II. Because of this halving of the diploid number of chromosomes, meiosis is often referred to as a reduction division.
Meiosis is a continuum composed of two phases: the homologous chromosomes separate during meiosis I, and the chromatids separate during meiosis II. Prior to the start of meiosis I, the chromosomes duplicate so that the cells have 23 pairs of duplicated chromosomes (i.e., each chromosome has two chromatids)—or 4N DNA. During prophase of the first meiotic division, homologous pairs of chromosomes—22 pairs of autosomal chromosomes (autosomes) plus a pair of sex chromosomes—exchange genetic material through a process known as recombination or crossing over at attachment points known as chiasmata. This results in a random, but balanced, exchange of chromatid segments between the homologous maternal and paternal chromatids to produce recombinant homologous chromosomes comprising a mix of maternal and paternal DNA. At the completion of meiosis I, the daughter cells have a haploid number (23) of duplicated, crossed-over chromosomes—or 2N DNA.
During meiosis II, no additional duplication of DNA takes place. The chromatids simply separate so that each daughter receives a haploid number of unduplicated chromosomes—1N DNA. Gametes produced by this process are genetically different from each other and from either parent. The genetic diversity that arises from recombination during meiosis and the combining of gametes from different parental lineages causes significant phenotypic variation within the population, providing an efficient mechanism for adaptation and natural selection.
A major difference between male and female gametogenesis is that one spermatogonium yields four spermatids (see Fig. 53-2 B ), whereas one oogonium yields one mature oocyte and two or three polar bodies (see Fig. 53-2 C ). We discuss the details regarding timing and process for spermatogenesis on page 1100 , and for oogenesis on page 1120 .
Fusion of two haploid gametes, a mature spermatozoan from the father and a mature oocyte from the mother—referred to as fertilization —produces a new diploid cell with 2N DNA, a zygote, that will become a new individual.
The sex chromosomes that the parents contribute to the offspring determine the genotypic sex of that individual. The genotypic sex determines the gonadal sex, which in turn determines the phenotypic sex that becomes fully established at puberty. Thus, sex-determining mechanisms established at fertilization direct all later ontogenetic processes (processes that lead to the development of an organism) involved in male-female differentiation.
Fusion of a sperm and an egg—two haploid germ cells—results in a zygote, which is a diploid cell containing 46 chromosomes (see Fig. 53-1 ): 22 pairs of somatic chromosomes (autosomes) and a single pair of sex chromosomes. In females, these sex chromosomes are both X chromosomes, whereas males have one X and one Y chromosome.
When the karyotypes of normal females and males are compared, two differences are apparent. First, among the 23 pairs of chromosomes in females, 8 pairs—including the 2 X chromosomes—are of similar size, whereas males have only such pairs. Second, instead of a second X chromosome, males have a Y chromosome that is small and acrocentric (i.e., the centromere is located at one end of the chromosome): this chromosome is the only such chromosome that is not present in females.
In the offspring, 23 of the chromosomes—including 1 of the sex chromosomes—are from the mother, and 23—including the other sex chromosome—come from the father. Thus, the potential offspring has a unique complement of chromosomes differing from those of both the mother and the father. The ovum provided by the mother (XX) always provides an X chromosome. Because the male is the heterogenetic (XY) sex, half the spermatozoa are X bearing whereas the other half are Y bearing. Thus, the type of sperm that fertilizes the ovum determines the sex of the zygote. X-bearing sperm produce XX zygotes that develop into females with a 46,XX karyotype, whereas Y-bearing sperm produce XY zygotes that develop into males with a 46,XY karyotype. The genotypic sex of an individual is determined at the time of fertilization. The Y chromosome appears to be the fundamental determinant of sexual development. When a Y chromosome is present, the individual develops as a male; when the Y chromosome is absent, the individual develops as a female. In embryos with abnormal sex chromosome complexes, the number of X chromosomes is apparently of little significance.
The indifferent gonad is composed of an outer cortex and an inner medulla. In embryos with an XY sex chromosome complement (i.e., 46,XY), the medulla differentiates into a testis and the cortex regresses. On the other hand, in embryos with an XX sex chromosome complement (i.e., 46,XX), the cortex develops into an ovary and the medulla regresses. Thus, the Y chromosome exerts a powerful testis-determining effect on the indifferent gonad. In the absence of a Y chromosome, the indifferent gonad develops into an ovary.
Interestingly, two X chromosomes are necessary for normal ovarian development. In individuals with the karyotype 45,XO— Turner syndrome —the ovaries fail to develop fully and appear as streaks on the pelvic sidewall ( Box 53-1 ). Even the absence of only some genetic material from one X chromosome in XX individuals (e.g., due to chromosome breakage or deletion) may cause abnormal gonadal differentiation. However, a complete Y chromosome is necessary for development of the testes. Indeed, individuals with the karyotype 47,XXY— Klinefelter syndrome —are not phenotypic females (based on the presence of two X chromosomes) but males. Taken together, the data on 45,XO and 47,XXY individuals tell us that the absence of a Y chromosome causes female phenotypic development.
The best-known example of gonadal dysgenesis is a syndrome referred to as Turner syndrome, a disorder of the female sex characterized by short stature, primary amenorrhea, sexual infantilism, and certain other congenital abnormalities. Cells in these individuals have a 45,XO karyotype (i.e., they lack one of the X chromosomes). The gonads of individuals with Turner syndrome appear as firm, flat, glistening streaks (referred to as streak gonads) lying below the fallopian tubes with no evidence of either germinal or secretory elements. Instead, they are largely composed of connective tissue arranged in whorls suggestive of ovarian stroma. Individuals with Turner syndrome have normal female differentiation of both the internal and external genitalia, although these genitalia are usually small and immature.
Turner syndrome can also be caused by partial deletion of the X chromosome, particularly if the entire short arm of the X chromosome is missing, or by formation of an X-chromosome ring that develops as a result of a deletion and subsequent joining of the two free ends of the chromosome.
In at least half of affected individuals, Turner syndrome is caused by the total absence of one X chromosome. In others, the lesion is structural (i.e., partial deletion or ring chromosome). In at least a third of cases, the genetic lesion appears as part of a mosaicism; that is, some of the cells carry the aberrant or absent chromosome, whereas the rest are normal.
We have just seen that the absence of a Y chromosome and the presence of two complete X chromosomes lead to normal ovarian development. Why? The X chromosome is far larger than the Y chromosome (see Fig. 53-1 ) and contains nearly 10% of the human genome compared to <100 genes on the Y chromosome. Thus, the large number of X-linked diseases—affecting such processes as blood clotting and color vision—is hardly surprising. Compared with males, females have a double dose of X-chromosome genes. To avoid an overdosage of X-derived gene products, each somatic 46,XX cell at the blastocyst stage separately and randomly inactivates either the maternal or paternal X chromosome in a process called lyonization. Once inactivated, that X chromosome remains inactivated for the life of the cell and all of its descendants. The inactivated X chromosome is visible at interphase as a small dark dot of condensed chromatin in the nucleus known as the Barr body. Presence of a Barr body can be used to determine the genotypic sex of a cell. If one X chromosome is normally inactivated in females, then why are two X chromosomes necessary for normal ovarian development, as evidenced by the deficiencies in 45,XO individuals? The answer is that many genes on the inactivated X chromosome somehow are not silenced and are necessary for normal ovarian development.
With rare exceptions (see below), a Y chromosome ( Fig. 53-3 A ) is necessary for normal testicular development. Thus, it stands to reason that the gene that determines organogenesis of the testis is normally located on the Y chromosome. This so-called testis-determining factor (TDF) has been mapped to the short arm of the Y chromosome and indeed turns out to be a single gene called SRY (for sex-determining region Y ). The SRY gene encodes a transcription factor that belongs to the high-mobility group (HMG) superfamily of transcription factors. The family to which SRY belongs is evolutionarily ancient. One portion of the SRY protein, the 80–amino-acid HMG box, which actually binds to the DNA—is highly conserved among members of the family.
Rarely, the TDF may also be found translocated on other chromosomes. One example is a 46,XX male (see Fig. 53-3 B ), an individual whose sex chromosome complement is XX but whose phenotype is male. During normal male meiosis, human X and Y chromosomes pair and recombine at the distal end of their short arms. It appears that most 46,XX males arise as a result of an aberrant exchange of paternal genetic material between X and Y chromosomes during spermatogenesis. In such cases, the TDF is transferred from a Y chromatid to an X chromatid. If the sperm cell that fertilizes the ovum contains such an X chromosome with a TDF, the resultant individual will be a 46,XX male.
Just as an individual's genes determine whether the indifferent gonad develops into an ovary or a testis, so does the sex of the gonad dictate the gonad's endocrine and paracrine functions. Normally, chemical messengers—both endocrine and paracrine—produced by the gonad determine the primary and secondary sexual phenotypes of the individual. However, if the gonads fail to produce the proper messengers, if other organs (e.g., the adrenal glands) produce abnormal levels of sex steroids, or if the mother is exposed to chemical agents (e.g., synthetic progestins, testosterone) during pregnancy, sexual development of the fetus may deviate from that programmed by the genotype. Therefore, genetic determination of sexual differentiation is not irrevocable; numerous internal and external influences during development may modify or completely reverse the phenotype of the individual, whatever the genotypic sex ( Box 53-2 ).
Discordance between genotypic and phenotypic sex are referred to as disorders of sex development (DSD), a term that describes congenital conditions in which development of chromosomal, gonadal, or anatomical sex is atypical. The term DSD avoids gender labeling in the diagnosis as well as names with negative social connotation (e.g., hermaphrodite, pseudohermaphrodite, intersex) that some patients and parents may perceive to be harmful.
Most DSD conditions are caused by aberrant expression of SRY. For example, a number of patients have no recognizable Y chromosome but do have testes. Some of these individuals are 46,XX and possess both male and female sex organs. Others have mixed gonadal dysgenesis —a testis in addition to a streak ovary—and a 45,XO karyotype. Some affected individuals have only one type of gonadal tissue but morphological characteristics of both sexes. All these patterns can result from mosaicisms (e.g., 46,XY/46,XX) or from translocation of the SRY gene (see Fig. 53-3 B )—which normally resides on the Y chromosome—to either an X chromosome or an autosome. A “normal” testis in the absence of a Y chromosome has never been reported.
Another group of individuals with a karyotype of 46,XY has pure gonadal dysgenesis —streak gonads, but no somatic features of XO. In the past investigators assumed that these individuals possessed an abnormal Y chromosome. Perhaps the SRY gene is absent or its expression is somehow blocked.
The primary sex organs of an individual are the gonads: testes in males and ovaries in females. During embryonic development, the gonads originate as bilateral swellings in the intermediate mesoderm (coelomic epithelium and the underlying urogenital mesenchyme) adjacent to the developing kidneys. Early on (approximately fifth week in humans; Fig. 53-4 A ), these gonadal ridges are identical in the two sexes and are referred to as the indifferent gonads (see Fig. 53-4 B ). They are composed of an outer cortex and an inner medulla (see Fig. 53-4 C ) and capable of becoming either testis (see Fig. 53-4 D ) or ovary (see Fig. 53-4 E ). The products of genes on the sex chromosomes determine whether each indifferent gonad differentiates into a testis or an ovary. Thus, genotypic sex determines gonadal sex.
Germ cells —cells that give rise to gametes—play a key role in sexual differentiation by affecting gonad development. The primordial germ cells (PGCs) do not originate in the gonad; instead, they migrate to the gonad from the yolk sac along the mesentery of the hindgut at about the fifth week of embryo development (see Fig. 53-4 A, B ). The PGCs of humans are first found in the endodermal epithelium of the yolk sac in the vicinity of the allantoic stalk, and from there the germ cells migrate into the adjoining mesenchyme. During their journey they divide by mitosis. They eventually take up their position embedded in the gonadal ridges. Gonadal development fails to progress normally in the absence of germ cells. Thus, any event that interferes with germ cell migration may cause abnormal gonadal differentiation.
The gonad forms from a portion of the coelomic epithelium, the underlying mesenchyme, and the PGCs that migrate from the yolk sac. At 5 weeks' development, a thickened area of coelomic epithelium develops on the medial aspect of the urogenital ridge as a result of proliferation of both the coelomic epithelium and cells of the underlying mesenchyme. This prominence, which forms on the medial aspect of the mesonephros, is known as the gonadal ridge (see Fig. 53-4 B, C ).
Migration of the PGCs to the gonadal ridge establishes the anlagen for the primordial gonad. The primordial gonad at this early stage of development consists of both a peripheral cortex and a central medulla (see Fig. 53-4 C ) and has the capacity to develop into either an ovary or a testis. The cortex and medulla have different fates in males and females. The genotypic sex of the embryo directs the sexual development of the gonads. In an embryo with a 46,XY karyotype, the medullary portion of the gonad develops to become a testis and the cortex regresses. Conversely, 46,XX germ cells stimulate development of the cortex of the early gonad to become an ovary and the medulla regresses.
In male embryos, PGCs migrate from the cortex of the gonad, in which they were originally embedded, into the primitive sex cords of the medulla. There the PGCs induce maturation of primitive sex cord structures, which become hollowed out (see Fig. 53-4 D ) and develop into the seminiferous tubules, including the Sertoli cells. The PGCs also give rise to spermatogonia (see p. 1100 ), the first cells in the pathway to mature sperm. Remnants of the primitive sex cords also form the rete testis, a system of thin, interconnected tubules that develop in the dorsal part of the gonad; they drain the seminiferous tubules into the efferent ductules, which develop from the adjoining tubules of the mesonephros (see pp. 1079–1080 ). These tubular structures establish a pathway from the male gonad to the mesonephric duct, which evolves into the outlet for sperm. At the same time, the cortex regresses to form a thin epithelial layer covering the coelomic surface of the testis, and mesenchymal cells take up residence among the sex cords and eventually become the Leydig cells of the testis. At around the 10th week of development, the Leydig cells respond to fetal pituitary and placental hormones (mainly human chorionic gonadotropin; see p. 1111 ) by producing testosterone, which influences the differentiation of the external genitalia.
The main cell types within the seminiferous tubules are Sertoli cells and spermatogonia, which continue to divide by mitosis (albeit slowly) until puberty. At puberty the rate of spermatogonia division increases and a subgroup of spermatogonia begin meiosis and enter the process of spermatogenesis to produce mature sperm. A stem-cell population of spermatogonia is maintained by mitosis throughout the life of the male.
In female embryos, the medulla of the gonad regresses, the primary sex cords are resorbed, and the interior of the gonad is filled with a loose mesenchyme that is highly permeated by blood vessels. However, the cortex greatly increases in thickness, due to the investment of mitotically dividing PGCs, which remain embedded within it and give rise to oogonia (see Fig. 53-4 E ). By the eighth week the developing ovaries contain around 600,000 oogonia and that number increases to 6 to 7 million by week 20. A large number of oogonia die and become resorbed; the remainder become surrounded by a single layer of granulosa cells to form primordial follicles and enter meiosis to become primary oocytes (see pp. 1120–1121 ). Unlike spermatogonia, the entire investment of oogonia (surviving PGCs) in the developing ovary is irreversibly committed to meiosis by the 20th week of development. At this stage, the oocytes are arrested at prophase I of meiosis and remain in that state until the follicle is selected for maturation or death later in life. At birth, each ovary holds around 1 million primordial follicles, each containing one primary oocyte arrested at prophase I. Because all the oogonia are depleted at midgestation (they either die or become oocytes), the number of primordial follicles formed at that time is all that will be available for reproduction for the rest of the female's life. This process is distinct from spermatogenesis, which occurs continually after puberty due to the replenishment of spermatogonia by mitosis.
Higher vertebrates, including humans, have evolved elaborate systems of glands and ducts—collectively referred to as the accessory sex organs —for storing and transporting gametes. Together the gonads and accessory sex organs constitute the primary sex characteristics. The accessory sex organs can be divided into the external and internal components. In males the external organs are the penis and scrotum. Although they are outside the abdominal cavity, the testicles, contained in the scrotum, are usually considered internal organs. Other internal organs are the epididymis, vas deferens, seminal vesicles, ejaculatory ducts, prostate, and bulbourethral glands. In females the external organs include the vulva, labia, and clitoris; the internal organs are the vagina, uterus, and fallopian tubes.
Secondary sex characteristics are external specializations that are not essential for the production and movement of gametes; instead, they are primarily concerned with sex behavior and with the birth and nutrition of offspring. Examples include pubic hair and breasts. Not only do the sex steroids produced by the gonads affect the accessory sex organs, they also modulate the physiological state of the secondary sex characteristics toward “maleness” in the case of the testes and “femaleness” in the case of the ovaries.
The internal genital ducts and accessory sex organs are derived from embryonic duct systems—the wolffian ducts (or mesonephric ducts) and the müllerian ducts (or paramesonephric ducts)—and the urogenital sinus ( Fig. 53-5 A ). The genital ducts are an essential part of the genital organs and form the pathway by which the sex cells—ova and spermatozoa—move to the location of fertilization.
It is worth recalling that during mammalian embryogenesis, three sets of kidneys develop, two of which are transient. The pronephric kidney, which develops first, is so rudimentary that it never functions. However, the duct that connects the pronephric kidney to the urogenital sinus—the pronephric duct—eventually serves the same purpose for the second kidney, the mesonephric kidney or mesonephros, as it develops embryologically. Unlike the pronephric kidney, the mesonephros functions transiently as a kidney. It has glomeruli and renal tubules; these tubules empty into the wolffian duct (see Fig. 53-5 A ), which in turn carry fluid to the urogenital sinus. As discussed below, the mesonephros and its wolffian ducts will—depending on the sex of the developing embryo—either degenerate or develop into other reproductive structures. In addition to the wolffian ducts, a second pair of genital ducts, the müllerian ducts, will develop as invaginations of the coelomic epithelium on the lateral aspects of the mesonephros. The müllerian ducts run caudally and parallel to the wolffian ducts. In the caudal region, they cross ventral to the wolffian ducts and fuse to form a cylindrical structure, the uterovaginal canal. The third or metanephric kidney becomes the permanent mammalian kidney. Its excretory duct is the ureter. Early in development (<7 weeks) embryos of both sexes have wolffian and müllerian ducts (see Fig. 53-4 C and Fig. 53-5 A ). However, later in gestation (by the 10th week) only one of the duct systems survives in each sex: wolffian ducts in males and müllerian ducts in females.
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