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Journal articles on the topic 'Spermatogenesis'

To see the other types of publications on this topic, follow the link: Spermatogenesis.

Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2024

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1

Moretti, Elena, Giulia Collodel, Giuseppe Belmonte, Daria Noto, and Emanuele Giurisato. "Defective spermatogenesis and testosterone levels in kinase suppressor of Ras1 (KSR1)-deficient mice." Reproduction, Fertility and Development 31, no. 8 (2019): 1369. http://dx.doi.org/10.1071/rd18386.

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The aim of this study was to clarify the role of the protein kinase suppressor of Ras1 (KSR1) in spermatogenesis. Spermatogenesis in ksr1−/− mice was studied in testicular tissue and epididymal spermatozoa by light and transmission electron microscopy and by immunofluorescence using antibodies to ghrelin and 3β-hydroxysteroid dehydrogenase (3β-HSD). Blood testosterone levels were also assessed. ksr1−/− mice showed reduced epididymal sperm concentration and motility as compared with wild-type (wt) mice. Testis tissue from ksr1−/− mice revealed a prevalent spermatogenetic arrest at the spermatocyte stage; the interstitial tissue was hypertrophic and the cytoplasm of the Leydig cells was full of lipid droplets. Ghrelin signal was present in the seminiferous tubules and, particularly, in the interstitial tissue of wt mice; however, in ksr1−/− mice ghrelin expression was very weak in both the interstitial tissue and tubules. On the contrary, the signal of 3β-HSD was weak in the interstitial tissue of wt and strong in ksr1−/− mice. Testosterone levels were significantly increased in the blood of ksr1−/− mice (P<0.05) as compared with wt. The results obtained reveal the importance of the KSR scaffold proteins in the spermatogenetic process. The study of the molecular mechanisms associated with spermatogenetic defects in a mouse model is essential to understand the factors involved in human spermatogenesis.

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2

de Kretser, D. M., K. L. Loveland, A. Meinhardt, D. Simorangkir, and N. Wreford. "Spermatogenesis." Human Reproduction 13, suppl 1 (April 1, 1998): 1–8. http://dx.doi.org/10.1093/humrep/13.suppl_1.1.

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3

Nishimura, Hitoshi, and Steven W. L’Hernault. "Spermatogenesis." Current Biology 27, no. 18 (September 2017): R988—R994. http://dx.doi.org/10.1016/j.cub.2017.07.067.

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4

Rodriguez-Sosa, Jose R., and Ina Dobrinski. "Recent developments in testis tissue xenografting." REPRODUCTION 138, no. 2 (August 2009): 187–94. http://dx.doi.org/10.1530/rep-09-0012.

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Development of the mammalian testis and spermatogenesis involve complex processes of cell migration, proliferation, differentiation, and cell–cell interactions. Although our knowledge of these processes has increased in the last few decades, many aspects still remain unclear. The lack of suitable systems that allow to recapitulate and manipulate both testis development and spermatogenesisex situhas limited our ability to study these processes. In the last few years, two observations suggested novel strategies that will improve our ability to study and manipulate mammalian spermatogenesis: i) testis tissue from immature animals transplanted ectopically into immunodeficient mice is able to respond to mouse gonadotropins and to initiate and complete differentiation to the level where fertilization-competent sperm are obtained, and ii) isolated testis cells are able to organize and rearrange into seminiferous cords that subsequently undergo complete development, including production of viable sperm. The current paper reviews recent advances that have been obtained with both techniques that represent novel opportunities to explore testis development and spermatogenesis in diverse mammalian species.

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5

Guha, T., A. Q. Siddiqui, and P. F. Prentis. "Ultrastructure of primary spermatocyte in fish (Tilapia: Oreochromis niloticus): The synaptonemal complex." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 288–89. http://dx.doi.org/10.1017/s0424820100143067.

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The Primary Spermatocytes represent a stage in spermatogenesis when the first meiotic cell division occurs. They are derived from Spermatogonium or Stem cell through mitotic division. At the zygotene phase of meiotic prophase the Synaptonemal complex appears in these cells in the space between the paired homologous chromosomes. Spermatogenesis and sperm structure in fish have been studied at the electron microscope level in a few species? However, no work has yet been reported on ultrastructure of tilapia, O. niloticus, spermatozoa and spermatogenetic process. In this short communication we are reporting the Ultrastructure of Primary Spermatocytes in tilapia, O. niloticus, and the fine structure of synaptonemal complexes seen in the spermatocyte nuclei.

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6

Rahadi, Yustisiane Ruth, Tri Wahyu Suprayogi, Rahmi Sugihartuti, Kadek Rachmawati, and Hani Plumeriastuti. "Effect of taurine on histopathological features of spermatogenesis in seminiferous tubules of mice (Mus musculus) induced by paraquat." Ovozoa : Journal of Animal Reproduction 11, no. 2 (August 17, 2022): 66–71. http://dx.doi.org/10.20473/ovz.v11i2.2022.66-71.

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This study aimed to determine the effect of taurine on the enhancement of the spermatogenetic process in male mice (Mus musculus) induced by paraquat (PQ). Twenty-five male mice (Mus musculus) aged 2-3 months with a bodyweight of around 35 grams were divided randomly into five groups. The K + and the treatment group (P1, P2, and P3) mice were induced using PQ. PQ was given intraperitoneally (IP) twice a week for 21 consecutive days at a dose of 30 mg/kg BW. Two hours after the administration of PQ, P1, P2, and P3 groups were given taurine at a dose of 250, 500, and 1000 mg/kg BW/day for three weeks (Heidari et al., 2019). K- group was given distilled water (IP) only. On day-29, mice were sacrificed for testicles histopathological preparations with hematoxylin-eosin staining. Results showed that the mice exposed to PQ only (the K+ group) had a reduced spermatogenesis score compared to those of the K- group (p <0.05). Taurine treatment on PQ-exposed mice was followed by an increase spermatogenesis score. The optimal curative dose of taurine was 500 mg/kg (P2 group). However, a higher dose (1000 mg/kg BW) of taurine resulted in a decline in the spermatogenesis score than those of at the 500 mg/kg. It could be concluded that treatment with taurine could enhance the spermatogenetic process of male mice (Mus musculus) induced by PQ.

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7

Meccariello, Rosaria, Rosanna Chianese, Vincenza Ciaramella, Silvia Fasano, and Riccardo Pierantoni. "Molecular Chaperones, Cochaperones, and Ubiquitination/Deubiquitination System: Involvement in the Production of High Quality Spermatozoa." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/561426.

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Spermatogenesis is a complex process in which mitosis, meiosis, and cell differentiation events coexist. The need to guarantee the production of qualitatively functional spermatozoa has evolved into several control systems that check spermatogenesis progression/sperm maturation and tag aberrant gametes for degradation. In this review, we will focus on the importance of the evolutionarily conserved molecular pathways involving molecular chaperones belonging to the superfamily of heat shock proteins (HSPs), their cochaperones, and ubiquitination/deubiquitination system all over the spermatogenetic process. In this respect, we will discuss the conserved role played by the DNAJ protein Msj-1 (mouse sperm cell-specific DNAJ first homologue) and the deubiquitinating enzyme Ubpy (ubiquitin-specific processing protease-y) during the spermiogenesis in both mammals and nonmammalian vertebrates.

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8

Rodrigues, Ramon T. G. A., José R. S. Santos, Lilianne M. S. Azerêdo, Ediane F. Rocha, Maria A. M. Carvalho, Maria J. I. D. Portal, Otávio B. Sousa, and Danilo J. A. Menezes. "Influence of scrotal bipartition on spermatogenesis yield and sertoli cell efficiency in sheep." Pesquisa Veterinária Brasileira 36, no. 4 (April 2016): 258–62. http://dx.doi.org/10.1590/s0100-736x2016000400002.

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Abstract With the objective to assess the effect of scrotal bipartition on spermatogenesis in sheep, the testes were used from 12 crossbred rams of sheep farms in the municipality of Patos, Paraíba, Brazil, distributed into two groups: GI with six rams with scrotal bipartition, and GII with six rams without scrotal bipartition. The testicular biometry was measured and the testes were collected, fixed in Bouin and fragments were processed to obtain histological slides. The spermatogenesis yield and the Sertoli cell efficiency was estimated by counting the cells of the spermatogenetic line at stage one of the seminiferous epithelium cycle and the Sertoli cells. The results were submitted to analysis of variance with the ASSISTAT v.7.6 program and the mean values were compared by the Student-Newman-Keuls test (SNK) at 5% significance. The testicular biometric parameters did not show statistical difference (p>0.05) between the groups. The meiotic, spermatogenetic and Sertoli cell efficiency were higher in bipartitioned rams (p<0.05), while the mitotic yield did not differ (p>0.05) between GI and GII. The results indicated that there is superiority in the spermatogenetic parameters of bi-partitioned rams, suggesting that these sheep present, as reported in goats, indication of better reproductive indices.

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9

Gribbins, Kevin. "Reptilian spermatogenesis." Spermatogenesis 1, no. 3 (July 2011): 250–69. http://dx.doi.org/10.4161/spmg.1.3.18092.

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10

Akdeniz, Ekrem, Mehmet Emin Onger, Mustafa Suat Bolat, Fatih Firat, Metin Gur, Onder Cinar, Mustafa Bakirtas, Abdullah Acıkgoz, and Fikret Erdemir. "Effect of atorvastatin on spermatogenesis in rats: A stereological study." Tropical Journal of Pharmaceutical Research 19, no. 12 (March 15, 2021): 2609–14. http://dx.doi.org/10.4314/tjpr.v19i12.19.

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Purpose: To investigate the effects of oral atorvastatin on spermatogenesis in a rat model.Methods: Rats were equally assigned into control and study groups, the latter receiving atorvastatin (20 mg/kg/day). At the end of 12 weeks, spermatogenetic activity was evaluated using stereological and optical fractionator methods. Serum follicle-stimulating hormone (FSH), total testosterone (TT), and luteinizing hormone (LH) levels were measured using micro–ELISA kits. Total cholesterol, triglyceride (TG), low-density lipoprotein cholesterol (LDL - C), and high-density lipoprotein cholesterol levels were also measured by enzymatic colorimetric assays.Results: Testicular stereological analysis revealed that atorvastatin reduced Sertoli cell numbers (p < 0.001), spermatogonia (p < 0.001), spermatocytes (p < 0.001), and seminiferous tubule diameters (p < 0.001). LDL – C (p = 0.01) and TG (p = 0.01) values were significantly lower in the study group compared with the control group. There was no significant difference in FSH (p = 0.44), LH (p = 0.48),and TT (p = 0.06) levels between the groups.Conclusion: The findings show that atorvastatin causes deleterious effects on rat spermatogenesis. It should therefore be used with caution in clinical practice owing to its potential adverse effects, especially on male fertility. Keywords: Statin, Atorvastatin, Spermatogenesis, Stereology, Testis

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11

Yushin, Vladimir, and Alexander Ryss. "Sperm development and structure in Bursaphelenchus mucronatus (Nematoda: Aphelenchoidea: Aphelenchoididae)." Nematology 13, no. 4 (2011): 395–407. http://dx.doi.org/10.1163/138855410x526840.

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AbstractSpermatogenesis in Bursaphelenchus mucronatus, described using TEM, is similar to that of the 'rhabditid' nematodes. The development includes formation of complexes of fibrous bodies (FB) and membranous organelles (MO) which appear in spermatocytes; the complexes dissociate in the spermatids; the immature sperm contains separate FB and MO and transformation continues only after activation in the female gonoduct. The spermatheca contains mature spermatozoa as bipolar cells subdivided into one large pseudopod and a main cell body containing a nucleus without a nuclear envelope, numerous mitochondria and peripheral membranous organelles opening to the exterior via pores. Pale reticulate bodies appearing in the B. mucronatus spermatids have no analogies in other nematode spermatogeneous cells. An unusual feature of B. mucronatus spermatozoa is the presence of a very large knob-like projection on each MO marking the pole which joins to the sperm plasmalemma to form a specific pore during in utero spermatozoon activation. The spermatogenesis of B. mucronatus resembles that of Aphelenchoides blastophthorus, although transparent vesicles in spermatids and spermatozoa, filopodia with microtubule-like fibres of immature spermatozoa, eccentric nucleus and multiple pseudopods of the mature spermatozoa distinguish spermatogenesis of the latter from the former. Spermatogenesis includes distinct cytomorphological features that may possibly be used to separate the Bursaphelenchus species and trace their phylogenetic relations.

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12

TERADA, HIROSHI, KIMIO FUJITA, ATSUSHI OTSUKA, HITOSHI SHINBO, SOICHI MUGIYA, and SEIICHIRO OZONO. "Oral clonidine advances spermatogenesis in oligozoospermic patients with spermatogenetic maturation arrest." International Journal of Urology 12, no. 9 (September 2005): 815–20. http://dx.doi.org/10.1111/j.1442-2042.2005.01144.x.

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13

Zhang, J., R. Yan, C. Wu, H. Wang, G. Yang, Y. Zhong, Y. Liu, L. Wan, and A. Tang. "Spermatogenesis-associated 48 is essential for spermatogenesis in mice." Andrologia 50, no. 6 (April 26, 2018): e13027. http://dx.doi.org/10.1111/and.13027.

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14

Wang, Hao-Qi, Tian Wang, Fei Gao, and Wen-Zhi Ren. "Application of CRISPR/Cas Technology in Spermatogenesis Research and Male Infertility Treatment." Genes 13, no. 6 (June 1, 2022): 1000. http://dx.doi.org/10.3390/genes13061000.

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As the basis of animal reproductive activity, normal spermatogenesis directly determines the efficiency of livestock production. An in-depth understanding of spermatogenesis will greatly facilitate animal breeding efforts and male infertility treatment. With the continuous development and application of gene editing technologies, they have become valuable tools to study the mechanism of spermatogenesis. Gene editing technologies have provided us with a better understanding of the functions and potential mechanisms of action of factors that regulate spermatogenesis. This review summarizes the applications of gene editing technologies, especially CRISPR/Cas9, in deepening our understanding of the function of spermatogenesis-related genes and disease treatment. The problems of gene editing technologies in the field of spermatogenesis research are also discussed.

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15

RUSSELL, LONNIE D., and RALPH L. BRINSTER. "Ultrastructural Observations of Spermatogenesis Following Transplantation of Rat Testis Cells Into Mouse Seminiferous Tubules." Journal of Andrology 17, no. 6 (November 12, 1996): 615–27. http://dx.doi.org/10.1002/j.1939-4640.1996.tb01845.x.

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ABSTRACT: The testes of busulfan‐treated immunodeficient mice receiving seminiferous tubuie injections of testis cells from rats were examined by light and electron microscopy. The presence of active rat spermatogenesis was verified by criteria that are known to characterize spermatogenic cells of this species. In addition, spermatogenesis from the mouse was identified as taking place in some seminiferous tubules as the result of reinitiation of spermatogenesis after busulfan treatment. Rat spermatogenesis in mouse seminiferous tubules showed the generally recognized associations of cells known to characterize stages of spermatogenesis of the rat. The Sertoli cells associated with rat spermatogenesis were identified ultrastructurally as being of mouse origin. Thus, rat spermatogenesis, which has a cycle length that is 50% longer than mouse spermatogenesis, can proceed among mouse Sertoli cells, which supposedly exert much shorter cyclic influences in concert with mouse germ cell development. Studies are needed to determine if the timing of rat spermatogenesis is controlled by the germ cells or the Sertoli cells. These observations are considered preliminary since a thorough study of somatic‐germ cell relationships was not undertaken. It is concluded that a mouse Sertoli cell in the environment provided by the mouse testis can produce both mouse and rat gametes.

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16

Divya, V. "Dynamics of Spermatogenesis." Annual Research & Review in Biology 4, no. 1 (January 10, 2014): 38–50. http://dx.doi.org/10.9734/arrb/2014/4289.

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17

Sharpe, R. M. "Testosterone and spermatogenesis." Journal of Endocrinology 113, no. 1 (April 1987): 1–2. http://dx.doi.org/10.1677/joe.0.1130001.

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18

Song, Hye-Won, and Miles F. Wilkinson. "In vitro spermatogenesis." Spermatogenesis 2, no. 4 (October 2012): 238–44. http://dx.doi.org/10.4161/spmg.22069.

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19

O'Donnell, L. "Estrogen and Spermatogenesis." Endocrine Reviews 22, no. 3 (June 1, 2001): 289–318. http://dx.doi.org/10.1210/er.22.3.289.

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20

O’Donnell, Liza, Kirsten M. Robertson, Margaret E. Jones, and Evan R. Simpson. "Estrogen and Spermatogenesis*." Endocrine Reviews 22, no. 3 (June 1, 2001): 289–318. http://dx.doi.org/10.1210/edrv.22.3.0431.

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Abstract Although it has been known for many years that estrogen administration has deleterious effects on male fertility, data from transgenic mice deficient in estrogen receptors or aromatase point to an essential physiological role for estrogen in male fertility. This review summarizes the current knowledge on the localization of estrogen receptors and aromatase in the testis in an effort to understand the likely sites of estrogen action. The review also discusses the many studies that have used models employing the administration of estrogenic substances to show that male fertility is responsive to estrogen, thus providing a mechanism by which inappropriate exposure to estrogenic substances may cause adverse effects on spermatogenesis and male fertility. The reproductive phenotypes of mice deficient in estrogen receptors α and/or β and aromatase are also compared to evaluate the physiological role of estrogen in male fertility. The review focuses on the effects of estrogen administration or deprivation, primarily in rodents, on the hypothalamo-pituitary-testis axis, testicular function (including Leydig cell, Sertoli cell, and germ cell development and function), and in the development and function of the efferent ductules and epididymis. The requirement for estrogen in normal male sexual behavior is also reviewed, along with the somewhat limited data on the fertility of men who lack either the capacity to produce or respond to estrogen. This review highlights the ability of exogenous estrogen exposure to perturb spermatogenesis and male fertility, as well as the emerging physiological role of estrogens in male fertility, suggesting that, in this local context, estrogenic substances should also be considered “male hormones.”

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21

Trasler, Jacquetta M. "Epigenetics in spermatogenesis." Molecular and Cellular Endocrinology 306, no. 1-2 (July 10, 2009): 33–36. http://dx.doi.org/10.1016/j.mce.2008.12.018.

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22

Carreau, Serge, and Rex A. Hess. "Oestrogens and spermatogenesis." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1546 (May 27, 2010): 1517–35. http://dx.doi.org/10.1098/rstb.2009.0235.

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The role of oestrogens in male reproductive tract physiology has for a long time been a subject of debate. The testis produces significant amounts of oestrogenic hormones, via aromatase, and oestrogen receptors (ERs)α (ESR1) and ERβ (ESR2) are selectively expressed in cells of the testis as well as the epididymal epithelium, depending upon species. This review summarizes the current knowledge concerning the presence and activity of aromatase and ERs in testis and sperm and the potential roles that oestrogens may have in mammalian spermatogenesis. Data show that physiology of the male gonad is in part under the control of a balance of androgens and oestrogens, with aromatase serving as a modulator.

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23

White-Cooper, Helen, and Nina Bausek. "Evolution and spermatogenesis." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1546 (May 27, 2010): 1465–80. http://dx.doi.org/10.1098/rstb.2009.0323.

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Sexual reproduction depends on the production of haploid gametes, and their fusion to form diploid zygotes. Here, we discuss sperm production and function in a molecular and functional evolutionary context, drawing predominantly from studies in model organisms (mice, Drosophila , Caenorhabditis elegans ). We consider the mechanisms involved in establishing and maintaining a germline stem cell population in testes, as well as the factors that regulate their contribution to the pool of differentiating cells. These processes involve considerable interaction between the germline and the soma, and we focus on regulatory signalling events in a variety of organisms. The male germline has a unique transcriptional profile, including expression of many testis-specific genes. The evolutionary pressures associated with gene duplication and acquisition of testis function are discussed in the context of genome organization and transcriptional regulation. Post-meiotic differentiation of spermatids involves very dramatic changes in cell shape and acquisition of highly specialized features. We discuss the variety of sperm motility mechanisms and how various reproductive strategies are associated with the diversity of sperm forms found in animals.

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24

McDonough, Paul G., Hans J. Duvekot, and Ruud C. P. M. van Muyden. "Inhibition of Spermatogenesis." Fertility and Sterility 46, no. 2 (August 1986): 341–43. http://dx.doi.org/10.1016/s0015-0282(16)49542-7.

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25

O’Donnell, Liza, and Moira K. O’Bryan. "Microtubules and spermatogenesis." Seminars in Cell & Developmental Biology 30 (June 2014): 45–54. http://dx.doi.org/10.1016/j.semcdb.2014.01.003.

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26

Yan Cheng, C. "Biology of spermatogenesis." Seminars in Cell & Developmental Biology 29 (May 2014): 1. http://dx.doi.org/10.1016/j.semcdb.2014.04.031.

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27

Schulz, Rüdiger W., Luiz Renato de França, Jean-Jacques Lareyre, Florence LeGac, Helio Chiarini-Garcia, Rafael Henrique Nobrega, and Takeshi Miura. "Spermatogenesis in fish." General and Comparative Endocrinology 165, no. 3 (February 2010): 390–411. http://dx.doi.org/10.1016/j.ygcen.2009.02.013.

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28

Tüttelmann, Frank, Christian Ruckert, and Albrecht Röpke. "Disorders of spermatogenesis." medizinische genetik 30, no. 1 (February 26, 2018): 12–20. http://dx.doi.org/10.1007/s11825-018-0181-7.

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29

Xu, Chen, Ding Li, Jian Qiang Bao, Shao Feng Cao, and Yi Fei Wang. "MicroRNAs and Spermatogenesis." Biology of Reproduction 78, Suppl_1 (May 1, 2008): 54. http://dx.doi.org/10.1093/biolreprod/78.s1.54.

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30

Weidner, W., T. Diemer, and M. Bergmann. "Aging and spermatogenesis." Aging Health 2, no. 1 (February 2006): 53–58. http://dx.doi.org/10.2217/1745509x.2.1.53.

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31

Ma, Dan-Dan, Da-Hui Wang, and Wan-Xi Yang. "Kinesins in spermatogenesis†." Biology of Reproduction 96, no. 2 (February 2017): 267–76. http://dx.doi.org/10.1095/biolreprod.116.144113.

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32

SANYAL, S., P. B. PATRA, S. NAG, and N. M. BISWAS. "Indomethacin & Spermatogenesis." Andrologia 12, no. 2 (April 24, 2009): 179–85. http://dx.doi.org/10.1111/j.1439-0272.1980.tb00609.x.

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33

Silver, Lee M. "Spermatogenesis: Genetic aspects." Cell 52, no. 4 (February 1988): 485–86. http://dx.doi.org/10.1016/0092-8674(88)90461-8.

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34

Jankovic Velickovic, Ljubinka, and Vladisav Stefanovic. "Hypoxia and spermatogenesis." International Urology and Nephrology 46, no. 5 (November 22, 2013): 887–94. http://dx.doi.org/10.1007/s11255-013-0601-1.

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35

Stewart Irvine, D. "Assessment of spermatogenesis." Current Obstetrics & Gynaecology 2, no. 1 (March 1992): 20–26. http://dx.doi.org/10.1016/0957-5847(92)90006-w.

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36

Chirumbolo, Salvatore. "Resveratrol in spermatogenesis." Cell Biology International 39, no. 7 (February 26, 2015): 775–76. http://dx.doi.org/10.1002/cbin.10451.

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37

Johnson, Larry. "Efficiency of spermatogenesis." Microscopy Research and Technique 32, no. 5 (December 1, 1995): 385–422. http://dx.doi.org/10.1002/jemt.1070320504.

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38

Roveri, Antonella, Fulvio Ursini, Leopold Flohé, and Matilde Maiorino. "PHGPx and spermatogenesis." BioFactors 14, no. 1-4 (2001): 213–22. http://dx.doi.org/10.1002/biof.5520140127.

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39

Kotaja, Noora. "MicroRNAs and spermatogenesis." Fertility and Sterility 101, no. 6 (June 2014): 1552–62. http://dx.doi.org/10.1016/j.fertnstert.2014.04.025.

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40

Miura, Takeshi, Chiemi Miura, Yasuko Konda, and Kohei Yamauchi. "Spermatogenesis-preventing substance in Japanese eel." Development 129, no. 11 (June 1, 2002): 2689–97. http://dx.doi.org/10.1242/dev.129.11.2689.

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Under fresh-water cultivation conditions, spermatogenesis in the Japanese eel is arrested at an immature stage before initiation of spermatogonial proliferation. A single injection of human chorionic gonadotropin can, however, induce complete spermatogenesis, which suggests that spermatogenesis-preventing substances may be present in eel testis. To determine whether such substances exist, we have applied a subtractive hybridisation method to identify genes whose expression is suppressed after human chorionic gonadotropin treatment in vivo. We found one previously unidentified cDNA clone that was downregulated by human chorionic gonadotropin, and named it ‘eel spermatogenesis related substances 21’ (eSRS21). A homology search showed that eSRS21 shares amino acid sequence similarity with mammalian and chicken Müllerian-inhibiting substance. eSRS21 was expressed in Sertoli cells of immature testes, but disappeared after human chorionic gonadotropin injection. Expression of eSRS21 mRNA was also suppressed in vitro by 11-ketotestosterone, a spermatogenesis-inducing steroid in eel. To examine the function of eSRS21 in spermatogenesis, recombinant eSRS21 produced by a CHO cell expression system was added to a testicular organ culture system. Spermtogonial proliferation induced by 11-ketotestosterone in vitro was suppressed by recombinant eSRS21. Furthermore, addition of a specific anti-eSRS21 antibody induced spermatogonial proliferation in a germ cell/somatic cell co-culture system. We conclude that eSRS21 prevents the initiation of spermatogenesis and, therefore, suppression of eSRS21 expression is necessary to initiate spermatogenesis. In other words, eSRS21 is a spermatogenesis-preventing substance.

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Zhou, Yu, and Yunyan Wang. "Action and Interaction between Retinoic Acid Signaling and Blood–Testis Barrier Function in the Spermatogenesis Cycle." Cells 11, no. 3 (January 21, 2022): 352. http://dx.doi.org/10.3390/cells11030352.

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Spermatogenesis is a complex process occurring in mammalian testes, and constant sperm production depends on the exact regulation of the microenvironment in the testes. Many studies have indicated the crucial role of blood–testis barrier (BTB) junctions and retinoic acid (RA) signaling in the spermatogenesis process. The BTB consists of junctions between adjacent Sertoli cells, comprised mainly of tight junctions and gap junctions. In vitamin A-deficient mice, halted spermatogenesis could be rebooted by RA or vitamin A administration, indicating that RA is absolutely required for spermatogenesis. Accordingly, this manuscript will review and discuss how RA and the BTB regulate spermatogenesis and the interaction between RA signaling and BTB function.

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Cheng, C. Yan, and Dolores D. Mruk. "The biology of spermatogenesis: the past, present and future." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1546 (May 27, 2010): 1459–63. http://dx.doi.org/10.1098/rstb.2010.0024.

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The physiological function of spermatogenesis in Caenorhabditis elegans , Drosophila melanogaster and mammals is to produce spermatozoa (1n, haploid) that contain only half of the genetic material of spermatogonia (2n, diploid). This half number of chromosomes from a spermatozoon will then be reconstituted to become a diploid cell upon fertilization with an egg, which is also haploid. Thus, genetic information from two parental individuals can be passed onto their offspring. Spermatogenesis takes place in the seminiferous epithelium of the seminiferous tubule, the functional unit of the mammalian testis. In mammals, particularly in rodents, the fascinating morphological changes that occur during spermatogenesis involving cellular differentiation and transformation, mitosis, meiosis, germ cell movement, spermiogenesis and spermiation have been well documented from the 1950s through the 1980s. During this time, however, the regulation of, as well as the biochemical and molecular mechanisms underlying these diverse cellular events occurring throughout spermatogenesis, have remained largely unexplored. In the past two decades, important advancements have been made using new biochemical, cell and molecular biology techniques to understand how different genes, proteins and signalling pathways regulate various aspects of spermatogenesis. These include studies on the differentiation of spermatogonia from gonocytes; regulation of spermatogonial stem cells; regulation of spermatogonial mitosis; regulation of meiosis, spermiogenesis and spermiation; role of hormones (e.g. oestrogens, androgens) in spermatogenesis; transcriptional regulation of spermatogenesis; regulation of apoptosis; cell–cell interactions; and the biology of junction dynamics during spermatogenesis. The impact of environmental toxicants on spermatogenesis has also become an urgent issue in the field in light of declining fertility levels in males. Many of these studies have helped investigators to understand important similarities, differences and evolutionary relationships between C. elegans , D. melanogaster and mammals relating to spermatogenesis. In this Special Issue of the Philosophical Transactions of the Royal Society B: Biological Sciences , we have covered many of these areas, and in this Introduction , we highlight the topic of spermatogenesis by examining its past, present and future.

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Xiong, Yi, Chao Yu, and Qianting Zhang. "Ubiquitin-Proteasome System–Regulated Protein Degradation in Spermatogenesis." Cells 11, no. 6 (March 21, 2022): 1058. http://dx.doi.org/10.3390/cells11061058.

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Spermatogenesis is a prolonged and highly ordered physiological process that produces haploid male germ cells through more than 40 steps and experiences dramatic morphological and cellular transformations. The ubiquitin proteasome system (UPS) plays central roles in the precise control of protein homeostasis to ensure the effectiveness of certain protein groups at a given stage and the inactivation of them after this stage. Many UPS components have been demonstrated to regulate the progression of spermatogenesis at different levels. Especially in recent years, novel testis-specific proteasome isoforms have been identified to be essential and unique for spermatogenesis. In this review, we set out to discuss our current knowledge in functions of diverse USP components in mammalian spermatogenesis through: (1) the composition of proteasome isoforms at each stage of spermatogenesis; (2) the specificity of each proteasome isoform and the associated degradation events; (3) the E3 ubiquitin ligases mediating protein ubiquitination in male germ cells; and (4) the deubiquitinases involved in spermatogenesis and male fertility. Exploring the functions of UPS machineries in spermatogenesis provides a global picture of the proteome dynamics during male germ cell production and shed light on the etiology and pathogenesis of human male infertility.

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Chen, Yan, Xiaoliang Li, Huijuan Liao, Xiaotong Leung, Jiabei He, Xiang Wang, Fuping Li, Huanxun Yue, and Wenming Xu. "CFTR mutation compromises spermatogenesis by enhancing miR-15b maturation and suppressing its regulatory target CDC25A†." Biology of Reproduction 101, no. 1 (April 15, 2019): 50–62. http://dx.doi.org/10.1093/biolre/ioz062.

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Abstract MicroRNAs (miRNAs) have recently been shown to be important for spermatogenesis; both DROSHA and Dicer1 KO mice exhibit infertility due to abnormal miRNA expression. However, the roles of individual miRNAs in spermatogenesis remain elusive. Here we demonstrated that miR-15b, a member of the miR-15/16 family, is primarily expressed in testis. A miR-15b transgenic mouse model was constructed to investigate the role of miR-15b in spermatogenesis. Impaired spermatogenesis was observed in miR-15b transgenic mice, suggesting that appropriate expression of miR-15b is vital for spermatogenesis. Furthermore, we demonstrated that overexpression of miR-15b reduced CDC25A gene post-transcriptional activity by targeting the 3′-UTR region of CDC25A, thus regulating spermatogenesis. In vitro results further demonstrated that a mutation in CFTR could affect the interaction between Ago2 with Dicer1 and that Dicer1 activity regulates miR-15b expression. We extended our study to azoospermia patients and found that infertile patients have a significantly higher level of miR-15b in semen and plasma samples. Taken together, we propose that CFTR regulation of miR-15b could be involved in the post-transcriptional regulation of CDC25A in mammalian testis and that miR-15b is important for spermatogenesis.

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Li, Yanan, Xiang Liu, Xianghui Zhang, Hongyan Wang, Jianyang Chen, Jiankai Wei, Yubang Li, et al. "Single-Cell RNA Sequencing of the Testis of Ciona intestinalis Reveals the Dynamic Transcriptional Profile of Spermatogenesis in Protochordates." Cells 11, no. 24 (December 8, 2022): 3978. http://dx.doi.org/10.3390/cells11243978.

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Spermatogenesis is a complex and continuous process of germ-cell differentiation. This complex process is regulated by many factors, of which gene regulation in spermatogenic cells plays a decisive role. Spermatogenesis has been widely studied in vertebrates, but little is known about spermatogenesis in protochordates. Here, for the first time, we performed single-cell RNA sequencing (scRNA-seq) on 6832 germ cells from the testis of adult Ciona intestinalis. We identified six germ cell populations and revealed dynamic gene expression as well as transcriptional regulation during spermatogenesis. In particular, we identified four spermatocyte subtypes and key genes involved in meiosis in C. intestinalis. There were remarkable similarities and differences in gene expression during spermatogenesis between C. intestinalis and two other vertebrates (Chinese tongue sole and human). We identified many spermatogenic-cell-specific genes with functions that need to be verified. These findings will help to further improve research on spermatogenesis in chordates.

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HUANG, H. F. S., T. A. LINSENMEYER, R. ANESETTI, W. GIGLIO, J. E. OTTENWELLER, and L. POGACH. "Suppression and Recovery of Spermatogenesis Following Spinal Cord Injury in the Rat." Journal of Andrology 19, no. 1 (January 2, 1998): 72–80. http://dx.doi.org/10.1002/j.1939-4640.1998.tb02472.x.

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ABSTRACT: Recently, we reported that changes in spermatogenesis in adult rats during acute phase (within 2 weeks) of spinal cord injury (SCI) were associated with a suppression of pituitary‐testis hormone axis, and these effects mimic those that occur after hormone deprivation. In this study, we examined the long‐term (>4 weeks) effects of SCI on spermatogenesis and its recovery. Results of this study reveal that while serum follicle stimulating hormone, luteinizing hormone, and testosterone levels in SCI rats recovered within 1 month after the injury, their spermatogenesis continued to regress. By 3 months, spermatogenesis in 70% of SCI rats has totally regressed, characterized by the absence of proliferating spermatogonia; these effects could not be prevented by an otherwise effective regimen of testosterone treatment. Sertoli cells in the regressed seminiferous tubules exhibited unusual behavior, characterized by the formation of multiple cell layers and/or aggregates that extended into the tubular lumen. Active spermatogenesis was observed in nine of the 19 SCI rats by 6 months, seven of which had complete spermatogenesis, but with persisting abnormalities. These results demonstrate that SCI results in total, but reversible, regression of spermatogenesis. Failure to prevent such effects by an otherwise effective exogenous testosterone regimen suggests that non‐endocrine factors are involved in the SCI effects on spermatogenesis. The unusual Sertoli cell localization in the regressed testes may have been triggered by the loss of proliferating spermatogonia and may be involved in subsequent spermatogenic recovery.

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Wang, Li, Jingqian Wang, Xinming Gao, Chen Du, Congcong Hou, Chundan Zhang, Junquan Zhu, and Daojun Tang. "Characterization of Mitochondrial Prohibitin in Opsariichthys bidens and Its Potential Functions in Spermatogenesis." International Journal of Molecular Sciences 23, no. 13 (June 30, 2022): 7295. http://dx.doi.org/10.3390/ijms23137295.

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Spermatogenesis is the intricate and coordinated process by which spermatogonia develop into haploid differentiated spermatozoa. Mitochondria are essential for spermatogenesis, and prohibitin (PHB) is closely associated with mitochondrial structure and function during spermatogenesis. Although PHB has been implicated in spermatogenesis in some taxa, its roles in Opsariichthys bidens have not been determined. In this study, the expression patterns and potential functions of PHB in spermatogenesis in O. bidens were characterized using histological microscopic observations, PCR cloning, real-time quantitative PCR (qPCR), Western blotting (WB) and immunofluorescence (IF). The full-length cDNA of Ob-phb was 1500 bp encoding 271 amino acids. A sequence alignment demonstrated that the PHB protein is conserved among different animals. qPCR revealed that phb mRNA is widely distributed in O. bidens and highly expressed in the testes at stages IV and V. WB revealed that Ob-PHB is located in the mitochondria of testes. IF revealed the colocalization of PHB signals and mitochondria. Signals were detected around nuclei in spermatogonia and spermatocytes, gradually moving to the tail region during spermiogenesis, and finally aggregating in the midpiece. These results indicate that Ob-PHB was expressed in the mitochondria during spermatogenesis. In addition, this study proposed Ob-PHB may participate in the degradation of mitochondria and cell differentiation during spermatogenesis.

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McLachlan, R. I., C. Mallidis, K. Ma, S. Bhasin, and D. M. de Kretser. "Genetic disorders and spermatogenesis." Reproduction, Fertility and Development 10, no. 1 (1998): 97. http://dx.doi.org/10.1071/r98029.

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Male infertility affects one man in twenty and a genetic basis seems likely in at least 30% of those men. Genetic regulation of fertility involves the inter-related processes of testicular development, spermatogenesis (involving germ cell mitosis, meiosis and spermatid maturation), and their endocrine and paracrine regulation. In regard to spermatogenesis, particular attention has been given to the Yq11 region, where some spermatogenesis genes (‘azoospermia factors’) appear to be located. Several candidate genes have been identified but have not been shown to have a defined or essential role in spermatogenesis. Microdeletions of Yq11 are found in ~15% of azoospermic or severely oligospermic men. The complexity of the genetic control of male fertility is demonstrated by the evidence for genes involved in spermatogenesis and sexual differentiation on the X chromosome and autosomes. Better understanding of the genetic regulation of normal spermatogenesis will provide new probes for clinical studies; however, at present the majority of spermatogenic failure remains without an identified genetic linkage. The advent of intracytoplasmic sperm injection permits fertility in many previously sterile men and presents the possibility of their transmission of infertility; appropriate counselling is required.

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Hasbi, Hasbi, and Sri Gustina. "Androgen Regulation in Spermatogenesis to Increase Male Fertility." Indonesian Bulletin of Animal and Veterinary Sciences 28, no. 1 (March 3, 2018): 13. http://dx.doi.org/10.14334/wartazoa.v28i1.1643.

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<p class="00-6Abstrak2Wtz">Male fertility is affected by quantity and quality of sperm which controlled by androgens (testosterone and 5α-dihydrotestosterone) mediated by androgen receptors (AR). Androgen receptors belong to receptor group of steroid hormone and a group of ligand-activated nuclear receptor superfamily. This paper explains androgen hormone and its regulation in spermatogenesis to increase male fertility. Regulation of androgen hormone in spermatogenesis include initiation of spermatogenesis, proliferation and maturation of Sertoli cells, germ cell development, spermatogonia, meiosis, and spermiogenesis. The role of androgen hormone in regulation of spermatogenesis is influenced by AR, luteinizing hormone (LH), and follicle stimulating hormone (FSH) levels. Disruption of spermatogenesis will cause low male fertility. However, low concentrations of AR, LH and FSH could be enhanced by exogenous gonadotrophine releasing hormone (GnRH), LH, FSH, and testosterone to increase male fertility.</p>

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Rathi, R., A. Honaramooz, W. Zeng, R. Turner, and I. Dobrinski. "Germ cell development in equine testis tissue xenografted into mice." Reproduction 131, no. 6 (June 2006): 1091–98. http://dx.doi.org/10.1530/rep.1.01101.

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Grafting of testis tissue from immature animals to immunodeficient mice results in complete spermatogenesis, albeit with varying efficiency in different species. The objectives of this study were to investigate if grafting of horse testis tissue would result in spermatogenesis, and to assess the effect of exogenous gonadotropins on xenograft development. Small fragments of testis tissue from 7 colts (2 week to 4 years of age) were grafted under the back skin of castrated male immunodeficient mice. For 2 donor animals, half of the mice were treated with gonadotropins. Xenografts were analyzed at 4 and 8 months post-transplantation. Spermatogenic differentiation following grafting ranged from no differentiation to progression through meiosis with appearance of haploid cells. Administration of exogenous gonadotropins appeared to support post-meiotic differentiation. For more mature donor testis samples where spermatogenesis had progressed into or through meiosis, after grafting an initial loss of differentiated germ cells was observed followed by a resurgence of spermatogenesis. However, if haploid cells had been present prior to grafting, spermatogenesis did not progress beyond meiotic division. In all host mice with spermatogenic differentiation in grafts, increased weight of the seminal vesicles compared to castrated mice showed that xenografts were releasing testosterone. These results indicate that horse spermatogenesis occurs in a mouse host albeit with low efficiency. In most cases, spermatogenesis arrested at meiosis. The underlying mechanisms of this spermatogenic arrest require further investigation.

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