In addition to testes and ovaries, various internal accessory sex organs are needed for reproductive function. Most of these are derived from two systems of embryonic ducts. Male accessory organs are derived from the wolffian (mesonephric) ducts, and female accessory organs are derived from the mullerian (paramesonephric) ducts (fig. 20.5). Interestingly, the two duct systems are present in both male and female embryos between day 25 and day 50, and so embryos of both sexes have the potential to form the accessory organs characteristic of either sex.
Experimental removal of the testes (castration) from male embryonic animals results in regression of the wolffian ducts and development of the mullerian ducts into female accessory organs: the uterus and uterine (fallopian) tubes. Female accessory sex organs, therefore, develop as a result of the absence of testes rather than as a result of the presence of ovaries.
In a male, the Sertoli cells of the seminiferous tubules secrete mullerian inhibition factor (MIF), a polypeptide that causes regression of the mullerian ducts beginning at about day 60. The secretion of testosterone by the Leydig cells of the testes subsequently causes growth and development of the wolf-fian ducts into male accessory sex organs: the epididymis, ductus (vas) deferens, seminal vesicles, and ejaculatory duct.
The external genitalia of males and females are essentially identical during the first 6 weeks of development, sharing in common a urogenital sinus, genital tubercle, urethral folds, and a pair of labioscrotal swellings. The secretions of the testes masculinize these structures to form the penis and spongy (penile) urethra, prostate, and scrotum. In the absence of secreted testosterone, the genital tubercle that forms the penis in a male will become the clitoris in a female. The penis and clitoris are thus said to be homologous structures. Similarly, the labioscrotal swellings form the scrotum in a male or the labia majora in a female; these structures are therefore homologous also (fig. 20.6).
Developing ! penis
Developing glans clitoris
Glans clitoris Hymen
Developing glans clitoris
Labia minora Labia majora
Glans clitoris Hymen
■ Figure 20.6 The development of the external genitalia in the male and female. (a [ai, sagittal view]) At 6 weeks, the urethral fold and labioscrotal swelling have differentiated from the genital tubercle. (b) At 8 weeks, a distinct phallus is present during the indifferent stage. By week 12, the genitalia have become distinctly male (c) or female (d), being derived from homologous structures. (e, f) At 16 weeks, the genitalia are formed.
Masculinization of the embryonic structures described occurs as a result of testosterone secreted by the embryonic testes. Testosterone itself, however, is not the active agent within all of the target organs. Once inside particular target cells, testosterone is converted by the enzyme 5a-reductase into the active hormone known as dihydrotestosterone (DHT) (fig. 20.7). DHT is needed for the development and maintenance of the penis, spongy urethra, scrotum, and prostate. Evidence suggests that testosterone itself directly stimulates the wolffian duct derivatives—epididymis, ductus deferens, ejaculatory duct, and seminal vesicles.
In summary, the genetic sex is determined by whether a Y-bearing or an X-bearing sperm cell fertilizes the ovum; the
Reproduction presence or absence of a Y chromosome in turn determines whether the gonads of the embryo will be testes or ovaries; the presence or absence of testes, finally, determines whether the accessory sex organs and external genitalia will be male or female (table 20.1). This regulatory pattern of sex determina-
tion makes sense in light of the fact that both male and female embryos develop within an environment high in estrogen, which is secreted by the mother's ovaries and the placenta. If the secretions of the ovaries determined the sex, all embryos would be female.
■ Figure 20.7 The formation of DHT. Testosterone, secreted by the interstitial (Leydig) cells of the testes, is converted into dihydrotestosterone (DHT) within the target cells. This reaction involves the addition of a hydrogen (and the removal of the double carbon bond) in the first (A) ring of the steroid.
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