Spermatogenesis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Spermatogenesis is the process by which male spermatogonia develop into mature spermatozoa. Spermatozoa are the mature male gametes in many sexually reproducing organisms. Thus, spermatogenesis is the male version of gametogenesis. In mammals it occurs in the male testes and epididymis in a stepwise fashion, and for humans takes approximately 64 days.[1] Spermatogenesis is highly dependent upon optimal conditions for the process to occur correctly, and is essential for sexual reproduction. It starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age. The entire process can be broken up into several distinct stages, each corresponding to a particular type of cell:
| Cell type | ploidy/chromosomes | chromatids | Process |
| spermatogonium (types A and B) | diploid/46 | 2N | spermatocytogenesis (mitosis) |
| primary spermatocyte | diploid/46 | 4N | spermatidogenesis (meiosis 1) |
| secondary spermatocyte | haploid/23 | 2N | spermatidogenesis (meiosis 2) |
| spermatid | haploid/23 | 1N | spermiogenesis |
| sperm | haploid/23 | 1N | spermiation |
Purpose
Spermatogenesis produces mature male gametes, commonly called sperm but specifically known as spermatozoa, which are able to fertilize the counterpart female gamete, the oocyte, during conception to produce a single-celled individual known as a zygote. This is the cornerstone of sexual reproduction and involves the two gametes both contributing half the normal set of chromosomes (haploid) to result in a chromosomally normal (diploid) zygote.
To preserve the number of chromosomes in the offspring, which differs between species, each gamete must have half the usual number of chromosomes present in other body cells. Otherwise, the offspring will have twice the normal number of chromosomes, and serious abnormalities may result. In humans, chromosomal abnormalities arising from incorrect spermatogenesis can result in Down Syndrome, Klinefelter's Syndrome, and spontaneous abortion. Most chromosomally abnormal zygotes will not survive for long after conception; however, plant reproduction is a little more robust, and viable new species may arise from cases of polyploidy.
Location
Spermatogenesis takes place within several structures of the male reproductive system. The initial stages occur within the testes and progress to the epididymis where the developing gametes mature and are stored until ejaculation. The seminiferous tubules of the testes are the starting point for the process, where stem cells adjacent to the inner tubule wall divide in a centripetal direction—beginning at the walls and proceeding into the innermost part, or lumen—to produce immature sperm. Maturation occurs in the epididymis and involves the acquisition of a tail and hence motility.
Stages
Spermatocytogenesis
Spermatocytogenesis is the male form of gametocytogenesis and results in the formation of spermatocytes possessing half the normal complement of genetic material. In spermatocytogenesis, a diploid spermatogonium divides mitotically to produce a diploid intermediate cell called a primary spermatocyte. Each primary spermatocyte duplicates its DNA and subsequently undergoes meiosis I to produce two haploid secondary spermatocytes. This division implicates sources of genetic variation, such as random inclusion of either parental chromosomes, and chromosomal crossover, to increase the genetic variability of the gamete.
Each cell division from a spermatogonium to a spermatid is incomplete; the cells remain connected to one another by bridges of cytoplasm to allow synchronous development. It should also be noted that not all spermatogonia divide to produce spermatocytes, otherwise the supply would run out. Instead, certain types of spermatogonia divide to produce copies of themselves, thereby ensuring a constant supply of gametogonia to fuel spermatogenesis.
Spermatidogenesis
Spermatidogenesis is the creation of spermatids from secondary spermatocytes. Secondary spermatocytes produced earlier rapidly enter meiosis II and divide to produce haploid spermatids. The brevity of this stage means that secondary spermatocytes are rarely seen in histological preparations.
Spermiogenesis
During spermiogenesis, the spermatids begin to grow a tail, and develop a thickened mid-piece, where the mitochondria gather and form an axoneme. Spermatid DNA also undergoes packaging, becoming highly condensed. The DNA is packaged firstly with specific nuclear basic proteins, which are subsequently replaced with protamines during spermatid elongation. The resultant tightly packed chromatin is transcriptionally inactive. The Golgi apparatus surrounds the now condensed nucleus, becoming the acrosome. One of the centrioles of the cell elongates to become the tail of the sperm.
Maturation then takes place, which removes the remaining unnecessary cytoplasm and organelles. The excess cytoplasm, known as residual bodies, is phagocytosed by surrounding Sertoli cells in the testes. The resulting spermatozoa are now mature but lack motility, rendering them sterile. The mature spermatozoa are released from the protective Sertoli cells into the lumen of the seminiferous tubule in a process called spermiation.
The non-motile spermatozoa are transported to the epididymis in testicular fluid secreted by the Sertoli cells with the aid of peristaltic contraction. Whilst in the epididymis they acquire motility and become capable of fertilisation. However, transport of the mature spermatozoa through the remainder of the male reproductive system is achieved via muscle contraction rather than the spermatozoon's recently acquired motility.
Role of Sertoli cells
At all stages of differentiation, the spermatogenic cells are in close contact with Sertoli cells which are thought to provide structural and metabolic support to the developing sperm cells. A single Sertoli cell extends from the basement membrane to the lumen of the seminiferous tubule, although the cytoplasmic processes are difficult to distinguish at the light microscopic level.
Sertoli cells serve a number of functions during spermatogenesis, they support the developing gametes in the following ways:
- Maintain the environment necessary for development and maturation via the blood-testis barrier
- Secrete substances initiating meiosis
- Secrete supporting testicular fluid
- Secrete androgen-binding protein, which concentrates testosterone in close proximity to the developing gametes
- Secrete hormones effecting pituitary gland control of spermatogenesis, particularly the polypeptide hormone, inhibin
- Phagocytose residual cytoplasm left over from spermiogenesis
- They release Anti-Mulerian Factor which prevents formation of the Mulerian Duct / Oviduct.
Influencing factors
The process of spermatogenesis is highly sensitive to fluctuations in the environment, particularly hormones and temperature. Testosterone is required in large local concentrations to maintain the process, which is achieved via the binding of testosterone by androgen binding protein present in the seminiferous tubules. Testosterone is also produced by interstitial cells, also known as Leydig cells, which preside adjacent to the seminiferous tubules.
Seminiferous epithelium is sensitive to elevated temperature in humans and some other species, and will be adversely affected by temperatures as high as normal body temperature. Consequently, the testes are located outside the body in a sack of skin called the scrotum. The optimal temperature is maintained at 2°C (man) - 8°C (mouse) below body temperature. This is achieved by regulation of blood flow[2] and positioning towards and away from the heat of the body by the cremasteric muscle and the dartos smooth muscle in the scrotum.
Dietary deficiencies (such as vitamins B, E and A), anabolic steroids, metals (cadmium and lead), x-ray exposure, dioxin, alcohol, and infectious diseases will also adversely affect the rate of spermatogenesis.
Hormonal control
Hormonal control of spermatogenesis varies among species. In humans the mechanism are not completely understood, however it is known that initiation of spermatogenesis occurs at puberty due to the interaction of the hypothalamus, pituitary gland and Leydig cells. If the pituitary gland is removed, spermatogenesis can still be initiated by follicle stimulating hormone and testosterone.
Follicle stimulating hormone stimulates both the production of androgen binding protein by Sertoli cells, and the formation of the blood-testis barrier. Androgen binding protein is essential to concentrating testosterone in levels high enough to initiate and maintain spermatogenesis, which can be 20-50 times higher than the concentration found in blood. Follicle stimulating hormone may initiate the sequestering of testosterone in the testes, but once developed only testosterone is required to maintain spermatogenesis. However, increasing the levels of follicle stimulating hormone will increase the production of spermatozoa by preventing the apoptosis of type A spermatogonia. The hormone inhibin acts to decrease the levels of follicle stimulating hormone.
The Sertoli cells themselves mediate parts of spermatogenesis though hormone production. They are capable of producing the hormones estradiol and inhibin. The Leydig cells are also capable of producing estradiol in addition to their main product testosterone.
See also
References
- ↑ Heller, C.G. (1963). "Spermatogenesis in Man: An Estimate of Its Duration". Science. 140 (3563): 184–6. Unknown parameter
|coauthors=ignored (help); Unknown parameter|month=ignored (help) - ↑ Harrison, R.G. (1949). "Vascular Patterns of the Mammalian Testis and Their Functional Significance" (PDF). Journal of Experimental Biology: 304–16, plates 9 & 10. Unknown parameter
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Additional Resources
- "The testes and spermatogenesis". University of Wisconsin. 1998.
- "Factors affecting spermatogenesis in the stallion". Theriogenology. 48 (7): 1199-1216. 1997.
- BARDIN CW: Pituitary-testicular axis. In: YEN SS , JAFFEE RB , eds: Reproductive Endocrinology, 3rd ed. Philadelphia: WB Saunders, 1991
- CHAMBERS CV , SHAFER MA , ADGER H , et al: Microflora of the urethra in adolescent boys: relationships to sexual activity and nongonococcal urethritis. J Ped 110:314-321, 1987
- CZYBA JC , GIROD C: Development of normal testis. In: HAFEZ ESE , ed: Descended and Cryptorchid Testis. The Hague, Martinus Nijhoff, 1980.
- Whitmore WF, Kars L, Gittes RF: The role of germinal epithelium and spermatogenesis in the privileged survival of intratesticular grafts. J Urol 1985;134:782.
External links
- Spermatogenesis - male reproductive physiology - Am Fam Physician 2000;62:1095.
Template:Male reproductive system Template:Reproductive physiology
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