Spermatocyte

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The process of spermatogenesis as the cells progress from spermatogium, to primary spermatocytes, to secondary spermatocytes, to spermatids, to Sperm
Schematic diagram of Spermatocytogenesis

Spermatocytes are a type of male gametocyte in animals. They derive from immature germ cells called spermatogonia. They are found in the testis, in a structure known as the seminiferous tubules. [1] There are two types of spermatocytes, primary and secondary. Through the process of spermatocytogenesis primary and secondary spermatocytes are formed. [2]

Primary spermatocytes are diploid (2N) cells containing 46 chromosomes. After Meiosis I, two secondary spermatocytes are formed. Secondary spermatocytes are haploid (N) cells that contain 23 chromosomes each.[1]

All male animals produce spermatocytes even, hermaphrodites such as C. elegans, which exist as a male or hermaphrodite. In hermaphrodite C. elegans, sperm production occurs first and is then stored in the spermatheca. Once the eggs are formed they are able to self-fertilize and produce up to 350 progenies. [3]

Formation[edit]

At puberty, spermatogonia located along the walls of the seminiferous tubules within the testis, will be initiated and start to divide mitotically forming two types of A cells; one is dark (Ad) and the other is pale (Ap). The Ad cells are spermatogonia that will stay in the basal compartment (outer region of the tubule); these cells are created to replenish the spermatogonia stores. Type Ap cells will mature and become type B cells. Type B cells will move on to the adluminal compartment (towards the inner region of tubule) and become primary spermatocytes; this process takes about 16 days to complete. [2][4]

The primary spermatocytes within the adluminal compartment will continue on to Meiosis I and divide into two daughters cells, also known as secondary spermatocytes, which takes 24 days to complete. Each secondary spermatocyte will form two spermatids after Meiosis II.[1]

Spermatogonia going through mitosis to form primary spermatocytes in Grasshopper testes.

Endocrine initiation[edit]

The formation of primary spermatocytes (a process known as spermatocytogenesis) in humans begins when a male is sexually matured at puberty around the age of 10 through 14.[5] It is initiated upon the pulsated surges of gonadotropin-releasing hormone (GnRH) from the hypothalamus, which leads to the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) produced by the anterior pituitary gland. The release of FSH into the testes will enhance spermatogenesis and lead to the development of sertoli cells, which act as nursing cells where spermatids will go to mature after Meiosis II. LH promotes leydig cells to secrete testosterone into the testes and blood inducing spermatogenesis and the formation of secondary sex characteristics. From this point on, the secretion of FSH and LH (inducing production of testosterone) will stimulate spermatogenesis until the male dies. [6] Interestingly enough, by increasing the hormones FSH and LH in males will not increase the rate of spermatogenesis. Although with age, the rate of production will decrease even though the amount of hormone secreted is constant due to higher rates of degeneration of germ cells during meiotic prophase.[1]

Cell Type Summary[edit]

Here is a table with the summary of the ploidy for primary spermatocyte and secondary spermatocytes, including number of chromosomes, DNA copy number, number of chromatids, process entered by cell and duration of each process. In the following table, ploidy, copy number and chromosome/chromatid counts are for one cell generally prior to DNA synthesis and division (in G1 if applicable). Primary spermatocytes are arrested after DNA synthesis and prior to division. [1] [2]

Cell type ploidy/chromosomes in human DNA copy number/chromatids in human Process entered by cell Duration
primary spermatocyte diploid (2N) / 46 4C / 2x46 spermatocytogenesis (Meiosis I) 24 days
secondary spermatocyte haploid (N) / 23 2C / 46 spermatocytogenesis (Meiosis II) A few hours

History[edit]

The spermatogenesis process in mammals as a whole, involving cellular transformation, mitosis, and meiosis, has been well studied and documented from the 1950’s-1980’s. However, the past two decades have focused around increasing understanding of the regulation of spermatogenesis via genes, proteins, and signaling pathways, and the biochemical and molecular mechanisms involved in these processes. Most recently, the environmental effects on spermatogenesis has become a focus as infertility in men has become more prevalent.[7]

An important discovery in the spermatogenesis process was the identification of the seminiferous epithelial cycle in mammals—work by C.P. Leblound and Y. Clermont in 1952 that studied the spermatogonia, spermatocyte layers, and spermatids in rat seminiferous tubules. Another critical discovery was that of the hypothalamic-pituitary-testicular axis, which plays a role in spermatogenesis regulation; this was studied by R. M. Sharpe in 1994.[7]

Damage, Repair, and Failure[edit]

Spermatocytes regularly overcome meiotically induced double strand breaks in the prophase stage; these are likely caused by Spo11, an enzyme required in meiotic recombination. These double strand breaks are repaired by homologous recombination pathways and utilize RAD1 and γH2AX, which recognize double strand breaks and modify chromatin, respectively. As a result, double strand breaks in meiotic cells, unlike mitotic cells, do not typically lead to apoptosis, or cell death. [8]

It is known that heterozygous chromosomal rearrangements lead to spermatogenic disturbance or failure; however the molecular mechanisms that cause this are not as well known. It is suggested that a passive mechanism involving asynaptic region clustering in spermatocytes is a possible cause. Asynaptic regions are associated with BRCA1, kinase ATR, and γH2AX presence in pachytene spermatocytes. [9]

Specific Mutations[edit]

Wild-type spermatocyte progression compared to repro4 mutated spermatocytes.

Stra8 is a gene required for retinoic-acid signaling pathway in humans, which leads to meiosis initiation. Stra8 expression is more present in preleptotene spermatocytes than spermatogonia. Stra8-mutant spermatocytes have been shown to be capable of meiosis initiation; however they cannot complete the process. Mutations in leptotene spermatocytes can result in premature chromosome condensation. [10]

Mutations in Mtap2, a microtubule-associated protein, as observed in repro4 mutant spermatocytes, have been shown to arrest spermatogenesis progress during the prophase of Meiosis I. This is observed by a reduction in spermatid presence in repro4 mutants.[11]

Recombinant-defective mutations can occur in Spo11, Dmc1, Atm, and Msh5 genes of spermatocytes. These mutations involve double strand break repair impairment, which can result in arrest of spermatogenesis at stage IV of the seminiferous epithelium cycle.[12]

Unique Properties in different species[edit]

Primary cilia is a common organelle found in eukaryotic cells. They play an important role in development of animals. Drosophila have unique properties in their spermatocyte primary cilia. It is assembled by four centrioles independently in the G2 phase and is sensitive to microtubule targeting drugs. Normally, primary cilia will develop from one centriole in the G0/G1 phase and are not effected by microtubule targeting drugs. [13]

Mesostoma ehrenbergii is a rhabdocoel flatworm with a distinctive male meiosis stage within the formation of spermatocytes. During the pre-anaphase stage, cleavage furrows are formed in the spermatocyte cells containing four univalent chromosomes. By the end of the anaphase stage, there is a one at each pole moving between the spindle poles without actually having physical interactions with one another (also known as distance segregation). These unique traits allows researchers to study the force created by the spindle poles to allow the chromosomes to move, cleavage furrow management and distance segregration. [14] [15]

See also[edit]

References[edit]

  1. ^ a b c d e Boron, Walter F., MD, Ph.D., Editor; Boulpaep, Emile L. (2012). "54". Medical physiology a cellular and molecular approach (Print) (Updated second ed.). Philadelphia: Saunders Elsevier. ISBN 9781437717532. 
  2. ^ a b c Schöni-Affolter, Dubuis-Grieder, Strauch, Franzisk, Christine, Erik Strauch. "Spermatogenesis". Retrieved 22 March 2014. 
  3. ^ Riddle, DL; Blumenthal, T; Riddle, B.J., editors. (1997). "I, The Biological Model". C. elegans II (2nd ed.). Cold Spring Harbor. NY: Cold Spring Harbor Laboratory Press. Retrieved April 13, 2014. 
  4. ^ Y, Clermont (1966). Renewal of spermatogonia in man. American Journal of Anatomy. p. 509–524. 
  5. ^ Starr, Taggart, Evers, Starr, Cecie, Ralph, Christine, Lisa (January 1, 2012). Animal Structure & Function. Cengage Learning. p. 736. ISBN 9781133714071. 
  6. ^ Sherwood, Lauralee (2010). Human physiology : from cells to systems (7th ed. ed.). Australia: Brooks/Cole, Cengage Learning. p. 751. ISBN 0495391840. 
  7. ^ a b Cheng, C. Yan; Dolores D. Mruk (19 April 2010). "The biology of spermatogenesis: the past, present and future". Phil. Trans. R. Soc. B. 1546 365: 1459-1463. Retrieved 23 April 2014. 
  8. ^ Matulis, Shannon; Mary Ann Handel. "Spermatocyte Responses In Vitro to Induced DNA Damage". Molecular Reproduction and Development (73): 1061-1072. Retrieved 9 April 2014. 
  9. ^ Sciurano, R. B.; M.I. Rahn, G. Rey-Valzacchi, R. Coco, A.J. Solari (21 August 2011). "The role of asynapsis in human spermatocyte failure". International Journal of Andrology (35): 541-549. Retrieved 9 April 2014. 
  10. ^ Mark, Manuel; Hugues Jacobs, Mustapha Oulad-Abdelghani, Chriistine Dennefeld, Betty Feret, Nadege Vernet, Carmen-Alina Codreanu, Pierre Chambon, Norbert Ghyselinck (7 July 2008). "STRA8-deficient spermatocytes initiate, but fail to complete, meiosis and undergo premature chromosome condensation". Journal of Cell Science 121: 3233-3242. 
  11. ^ Sun, Fengyun; Mary Ann Handel (10 January 2011). "A Mutation in Mtap2 is Associated with Arrest of Mammalian Spermatocytes before the First Meiotic Division". Genes 2: 21-35. 
  12. ^ Barchi, Marco; S. Mahadevaiah, M. Di Giacomo, F. Baudat, D. de Rooij, P. Burgoyne, M. Jasin, S. Keeney (August 2005). "Surveillance of Different Recombination Defects in Mouse Spermatocytes Yields Distinct Responses despite Elimination at an Identical Developmental Stage". Molecular and Cellular Biology: 7203-7215. 
  13. ^ Riparbelli, MG; Cabrera, OA; Callaini, G; Megraw, TL (2013). "Unique properties of Drosophila spermatocyte primary cilia.". Biology open 2 (11): 1137–47. PMID 24244850. Retrieved 21 April 2014. 
  14. ^ Ferraro-Gideon, Jessica; Hoang, Carina; Forer, Arthur (7 August 2013). "Meiosis-I in Mesostoma ehrenbergii spermatocytes includes distance segregation and inter-polar movements of univalents, and vigorous oscillations of bivalents". Protoplasma 251 (1): 127–143. doi:10.1007/s00709-013-0532-9. Retrieved 22 April 2014. 
  15. ^ Ferraro-Gideon, J; Hoang, C; Forer, A (2013 Sep). "Mesostoma ehrenbergii spermatocytes--a unique and advantageous cell for studying meiosis.". Cell biology international 37 (9): 892–8. PMID 23686688. Retrieved 22 April 2014. 

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