Spermatocytes are a type ofmalegametocyte in animals. They derive from immaturegerm cells calledspermatogonia. They are found in thetestis, in a structure known as theseminiferous tubules.[1] There are two types of spermatocytes, primary and secondary spermatocytes. Primary and secondary spermatocytes are formed through the process ofspermatocytogenesis.[2]
Primary spermatocytes arediploid (2N) cells. Aftermeiosis I, two secondary spermatocytes are formed. Secondary spermatocytes arehaploid (N) cells that contain half the number of chromosomes.[1]
In all animals,males produce spermatocytes, evenhermaphrodites such asC. elegans, which exist as a male or hermaphrodite. In hermaphroditeC. elegans, sperm production occurs first and is then stored in thespermatheca. Once theeggs are formed, they are able to self-fertilize and produce up to 350progeny.[3]
_Grasshopper_testes_(Spermatogonia).jpg)
Atpuberty,spermatogonia located along the walls of theseminiferous tubules within thetestis will be initiated and start to dividemitotically, forming two types of A cells that contain an oval shaped nucleus with a nucleolus attached to the nuclear envelope; 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 reservespermatogonial stem cells that do not usually undergo mitosis. Type Ap are actively-dividingspermatogonial stem cells which begin differentiation to type B spermatogonia, which have round nuclei and heterochromatin attached to the nuclear envelope and the center of nucleolus.[4] 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][5]
The primary spermatocytes within the adluminal compartment will continue on tomeiosis I and divide into two daughters cells, known as secondary spermatocytes, a process which takes 24 days to complete. Each secondary spermatocyte will form twospermatids aftermeiosis II.[1]
Although spermatocytes that divide mitotically and meiotically are sensitive toradiation andcancer,spermatogonial stem cells are not. Therefore, after termination ofradiation therapy orchemotherapy, the spermatognia stems cells may re-initiate the formation of spermatogenesis.[6]
The formation of primary spermatocytes (a process known asspermatocytogenesis) begins in humans when a male is sexually matured atpuberty, around the age of 10 through 14.[7] Formation is initiated upon the pulsated surges ofgonadotropin-releasing hormone (GnRH) from thehypothalamus, which leads to the secretion offollicle-stimulating hormone (FSH) andluteinizing hormone (LH) produced by theanterior pituitary gland. The release of FSH into the testes will enhance spermatogenesis and lead to the development ofSertoli cells, which act as nursing cells wherespermatids will go to mature aftermeiosis II. LH promotesLeydig cell secretion oftestosterone into the testes and blood, which induce spermatogenesis and aid the formation of secondary sex characteristics. From this point on, the secretion of FSH and LH (inducing production of testosterone) will stimulatespermatogenesis until the male dies.[8] Increasing thehormones FSH and LH in males will not increase the rate of spermatogenesis. However, with age, the rate of production will decrease, even when the amount of hormone that is secreted is constant; this is due to higher rates of degeneration ofgerm cells duringmeioticprophase.[1]
In the following table, ploidy, copy number and chromosome/chromatid counts listed are for a single 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 |
|---|---|---|---|---|---|
| spermatogonium (types Ad, Ap and B) | germ cells | diploid (2N) / 46 | 2C / 46 | spermatocytogenesis (mitosis) | 16 days |
| primary spermatocyte | malegametocyte | diploid (2N) / 46 | 4C / 2x46 | spermatocytogenesis (meiosis I) | 24 days |
| secondary spermatocyte | male gametocyte | haploid (N) / 23 | 2C / 46 | spermatidogenesis (meiosis II) | A few hours |
| spermatids | malegametid | haploid (N) / 23 | 1C / 23 | spermiogenesis | 24 days |
| spermatozoids | sperm | haploid (N) / 23 | 1C / 23 | spermiation | 64 days (total) |
Spermatocytes regularly overcome double-strand breaks and otherDNA damages in the prophase stage ofmeiosis. These damages can arise by the programmed activity ofSpo11, an enzyme employed in meiotic recombination, as well as by un-programmed breakages in DNA, such as those caused byoxidative free radicals produced as products of normal metabolism. These damages are repaired by homologous recombination pathways and utilizeRAD1 and γH2AX, which recognize double strand breaks and modifychromatin, respectively. As a result, double strand breaks in meiotic cells, unlike mitotic cells, do not typically lead toapoptosis, or cell death.[9]Homologous recombinational repair (HRR) of double-strand breaks occurs in mice during sequential stages ofspermatogenesis but is most prominent in spermatocytes.[10] In spermatocytes, HRR events occur mainly in the pachytene stage of meiosis and thegene conversion type of HRR is predominant, whereas in other stages of spermatogenesis the reciprocal exchange type of HRR is more frequent.[10] During mouse spermatogenesis, themutation frequencies of cells at the different stages, including pachytene spermatocytes, are 5 to 10-fold lower than the mutation frequencies insomatic cells.[11] Because of their elevatedDNA repair capability, spermatocytes likely play a central role in the maintenance of these lower mutation rates, and thus in the preservation of the genetic integrity of the male germ line.
It is known thatheterozygous 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 withBRCA1, kinaseATR and γH2AX presence inpachytene spermatocytes.[12]
The gene Stimulated By Retinoic Acid 8 (STRA8) is required for the retinoic-acid signaling pathway in humans, which leads tomeiosis initiation.STRA8 expression is higher in preleptotene spermatocytes (at the earliest stage ofprophase I in meiosis) than inspermatogonia.STRA8-mutant spermatocytes have been shown to be capable of meiosis initiation; however, they cannot complete the process. Mutations inleptotene spermatocytes can result in premature chromosome condensation.[13]
Mutations inMtap2, amicrotubule-associated protein, as observed inrepro4 mutant spermatocytes, have been shown to arrest spermatogenesis progress during the prophase ofmeiosis I. This is observed by a reduction inspermatid presence inrepro4 mutants.[14]
Recombinant-defective mutations can occur inSpo11,DMC1,ATM andMSH5 genes of spermatocytes. These mutations involve double strand break repair impairment, which can result in arrest ofspermatogenesis at stage IV of the seminiferous epithelium cycle.[15]
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Thespermatogenesis process has been elucidated throughout the years by researchers who divided the process into multiple stages or phases, depending onintrinsic (germ and Sertoli cells) andextrinsic (FSH and LH) factors.[16] The spermatogenesis process in mammals as a whole, involving cellular transformation, mitosis, and meiosis, has been well studied and documented from the 1950s to 1980s. However, during the 1990s and 2000s researchers 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 have become a focus asmale infertility in men has become more prevalent.[17]
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 hormone chain, which plays a role in spermatogenesis regulation; this was studied by R. M. Sharpe in 1994.[17]
Primarycilia are commonorganelles found ineukaryotic cells; they play an important role in development of animals.Drosophila have unique properties in their spermatocyte primary cilia—they are assembled by fourcentrioles independently in theG2 phase and are sensitive tomicrotubule-targeting drugs. Normally, primary cilia will develop from one centriole in the G0/G1 phase and are not affected by microtubule targeting drugs.[18]
Mesostoma ehrenbergii is arhabdocoelflatworm with a distinctive malemeiosis stage within the formation of spermatocytes. During the pre-anaphase stage, cleavage furrows are formed in the spermatocyte cells containing four univalentchromosomes. By the end of theanaphase stage, there is 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 allow researchers to study the force created by the spindle poles to allow the chromosomes to move, cleavage furrow management and distance segregation.[19][20]