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This page introduces male gonad (testis) and reproductive tract development. The paired mesonephric ducts, also historically called Wolffian ducts, are preserved in male development and lost in females. The initial difference in male and female gonad development are dependent on testis-determining factor (TDF) the protein product of the Y chromosome SRY gene. Recent studies have indicated that additional factors may also be required for full differentiation. The seminiferous tubules are considered the parenchyma of the testis. (More? See also Spermatogenesis | SRY) |
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Male Gonad (testis) Development (228 Kb) |
Male External Genitalia (288 Kb) |
Testes Descent (172 Kb) |
(Clicking image or text will open movie, more movies can be seen on the Urogenital Movies page)
Page Links: Introduction | Some Recent Findings | Development Overview | Testicular Descent | Leydig Cells | Movies | References | Glossary
Other Pages: Y chromosome | Genital Abmormalities | Week 1 - Spermatogenesis | Endocrine Abnormalities | Endocrine Development - Pituitary
Wilhelm D, Palmer S, Koopman P. Sex determination and gonadal development in mammals. Physiol Rev. 2007 Jan;87(1):1-28. Review.
"We review here the molecular and cellular events (differentiation, migration, proliferation, and communication) that distinguish testis and ovary during fetal development, and the changes in gene regulation that underpin these two alternate pathways."
Toppari J, Virtanen H, Skakkebaek NE, Main KM. Environmental effects on hormonal regulation of testicular descent. J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):184-6. (More? Testicular Descent)
"Regulation of testicular descent is hormonally regulated, but the reasons for maldescent remain unknown in most cases."
The Y Chromosome contains approximately 200+ genes and consists of 50 million base pairs. Only 50% of its content has been determined. (More? Y chromosome)
Sex Determination
Gonad development
SRY
Internal Genital Organs
External Genital Organs
Leydig cells named after german zoologist Franz von Leydig (1821 - 1908). These cells produce the male testicular androgens and occur during life prenatally fetal and postnatally at puberty.
Fetal Leydig Cells
Have a hormonal role in male genitalia differentiation and are lost postnatally. These cells arise approximately at 6 weeks (human) and 12.5 dpc (mouse) and there appears to be differences in hormonal sensitivity between the species. Their initial differentiation requires both luteinizing hormone (LH) and adrenocorticotrophic hormone (ACTH) and therefore normal pituitary development.
(More? Endocrine Development - Pituitary)
Adult (Puberty) Leydig Cells
Have a hormonal role in puberty, secondary sex characteristics and sexual maturation. Their initial differentiation from peritubular mesenchymal cells does not require gonadotropin, but development and function are dependent upon luteinizing hormone (LH). The cells differentiate with three discrete stages (newly formed, immature, mature) leading to a decrease in proliferation and increasing testosterone biosynthetic capacity. Insulin-like growth factor I (IGF-I) stimulates proliferation of immature cells and promotes their maturation. Testosterone and estrogen inhibit the process of precursor cell differentiation and may be responsible for the cessation of proliferation in the adult Leydig cells.
(More? Leydig reviews)
Links: Franz von Leydig
Puberty - immature Sertoli cells cease to proliferate and differentiate.
Molecular factors: Follicle Stimulating Hormone (FSH) -> Krüppel-like factor 4 (KLF4)
Krüppel-like factor 4 (KLF4) - zinc finger transcription factor, terminal differentiation of epithelial cells.
Epidermal Growth Factor (EGF)
Transforming Growth Factor-beta (TGFbeta)
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In humans at puberty, hormonal and morphological changes occur within the gonad and other systems (secondary sex characteristics). Within the testis the immature Sertoli cells cease to proliferate and differentiate. Spermatogonium proliferate and spermatogenesis begins, and it takes about 70 days for cells to mature from the diploid spermatogonium to a primary spermatocyte. This maturation occurs in waves along the seminiferous tubules. |
Histology sections through the testis seminiferous tubule (Images: UWA Blue Histology) |
(More? Week 1 - Spermatogenesis)
More movies can be seen on the Urogenital Movies page.
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Male Gonad (testis) Development (228 Kb) |
Male External Genitalia (288 Kb) |
Testes Descent (172 Kb) |
(Clicking image or text will open movie)
This topic is also covered on Genital Abmormalities page.
Toppari J, Virtanen H, Skakkebaek NE, Main KM. Environmental effects on hormonal regulation of testicular descent. J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):184-6.
"Regulation of testicular descent is hormonally regulated, but the reasons for maldescent remain unknown in most cases. The main regulatory hormones are Leydig cell-derived testosterone and insulin-like factor 3 (INSL3). Luteinizing hormone (LH) stimulates the secretion of these hormones, but the secretory responses to LH are different: INSL3 secretion increases slowly and may reflect the LH dependent differentiated status of Leydig cells, whereas testosterone response to LH is immediate. Testosterone contributes to the involution of the suspensory ligament and to the inguinoscrotal phase of the descent, while INSL3 acts mainly in transabdominal descent by stimulating the growth of the gubernaculum. INSL3 acts through a G-protein coupled receptor LGR8. "
Kaleva M, Toppari J. Cryptorchidism: an indicator of testicular dysgenesis? Cell Tissue Res. 2005 Oct;322(1):167-72.
"Cryptorchidism is a common ailment of new-born boys, affecting 1-9% of full term boys at birth."
Fetal development of the human gubernaculum with special reference to the fasciae and muscles around it. Niikura H, Okamoto S, Nagase S, Takano T, Murakami G, Tatsumi H, Yaegashi N. Clin Anat. 2008 Sep;21(6):547-57. PMID: 18661576
"At 8-12 weeks of gestation, the gubernaculum arose from the mesonephric fold at or near the gonad. Gubernacular mesenchyme communicated with the subcutaneous tissue via a narrow slit in the rectus aponeurosis. The inguinal fold, containing the inferior epigastric vessels, was separated from the gubernaculum. At 20-25 weeks of gestation, the gubernaculum connected to the testis or uterus. When the testis successfully descended to a peritoneal recess on the lateral side of the umbilical artery, the gubernaculum connected to the testis free of interference by the thick artery and its associated peritoneal fold. This may explain the known asymmetry in testicular descent. The inguinal canal was enclosed by a sheet-like aponeurosis: its ventromedial part was composed of the rectus sheath and the external oblique aponeurosis, whereas the dorsolateral part consisted of a thick aponeurosis covering or facing the iliopsoas. The former (latter) aponeurosis seemed to develop into the inguinal ligament (the iliopubic tract) in adults. According to the topohistology of the muscles associated with the interfoveolar ligament, we identified muscle fragments around the gubernaculum as derivatives of the transversus and/or internal oblique. Consequently, the inguinal canal contained the cremaster proper developing within the gubernaculum and parts of the abdominal wall muscles mechanically incorporated into the canal."
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The male and female reproductive systems develop initially "indifferently", it is the product of the Y chromosome SRY gene that makes the difference.
Please email Dr Mark Hill if you wish to make a comment about this current project.
