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PubMed1987

The ultrastructure of normal fetal and neonatal pig testis germ cells and the influence of fetal decapitation on the germ cell development.

The development of germ cells in the male pig was investigated ultrastructurally in normal and decapitated fetuses. The age ranged respectively from 30 days p.c. till one month after birth and from 52 days p.c. until birth. The ultrastructural organization of the germ cells changes dramatically between 30 days p.c. and 52 days p.c. which coincides with the formation of 'true' sex cords. From 52 days p.c. onwards the morphology is rather stable: cells show a 'hydrated' appearance and typical cell bridges. There is no obvious difference in the ultrastructure of germ cells in decapitated animals, their normal littermates and control animals. Therefore germ cell development in the pig is likely to be insensitive to gonadotropins during the fetal period. The development of pig germ cells follows closely the pattern described for several species. Quantitatively there is an increase in the ratio of germ cell/Sertoli cell per cross sectional diameter in the decapitated animals.

Animals↗
PubMed2006

Xenopus Dead end mRNA is a localized maternal determinant that serves a conserved function in germ cell development.

Germ plasm formation is considered to define the first step in germ cell development. Xenopus Dead end represents a germ plasm specific transcript that is homologous to the previously characterized zebrafish dead end, which is required for germ cell migration and survival. XDead end mRNA localizes to the vegetal pole of Xenopus oocytes; in contrast to all other known germ plasm associated transcripts in Xenopus, XDead end is transported via the late transport pathway, suggesting a different mode of germ plasm restriction. Vegetal localization in the oocyte is achieved via a localization element mapping to a 251 nucleotide element in the 3'-UTR. This RNA sequence binds to a set of proteins characteristic for the late localization pathway and to one additional protein of 38 kDa. Inhibition of XDead end translation in Xenopus embryos results in a loss of primordial germ cells at tadpole stages of development. Early specification events do not seem to be affected, but the primordial germ cells fail to migrate dorsally and eventually disappear. This phenotype is very similar to what has been observed in the zebrafish, indicating that the role of XDead end in germ cell development has been conserved in evolution.

3' Untranslated Regions↗
PubMed2004

Histochemical in situ identification of bovine embryonic blood cells reveals differences to the adult haematopoietic system and suggests a close relationship between haematopoietic stem cells and primordial germ cells.

Cryostat sections of bovine embryos of exactly known age (obtained from artificial insemination), ranging from 32 to 60 days post-insemination, were treated with a wide range of antibodies directed against cell surface antigens or lineage-specific factors in order to demonstrate different types of fetal blood cells and their precursors. An antibody specific to bovine c-kit (bk-1) stained not only presumptive haematopoietic stem cells in the dorsal aorta and the embryonic liver, but also a subpopulation of putative primordial germ cells in the gonadal anlage, the latter being further characterised by a positive labelling with the lectins STA, WFA and WGA and a histochemical reaction for alkaline phosphatase. The antibody against CD 45, commonly regarded as a pan-leukocyte marker, reacted in the bovine embryo with different types of blood cells, as well as with presumptive vasculogenetic cells and a subpopulation of putative primordial germ cells. CD 61 immunoreaction proved to be a useful tool for demonstrating megakaryocytopoiesis in the embryonic liver, in addition to the lumen of blood vessels and the mesonephros. Staining with BM-2 was restricted to a single population of medium-sized, round to oval cells, forming small groups within the parenchymal strands of the liver. Characterised furthermore by a U-shaped nucleus, this BM-2-positive cell type apparently represents a developmental stage in the granulopoietic lineage. B-lymphocytopoiesis in the bovine liver was detected with antibodies directed against WC-4 and IgM, but not until day 58 post-insemination. Using antibodies to CD 14, no positive results could be obtained in embryonic tissues, although anti-CD 14-positive macrophages were easily recognised in lymph nodes of adult bovines. The antibody against CD 68, however, identified two populations of primitive macrophages in our samples. One population was located in parenchymal strands of the embryonic liver, probably acting as nursing cells for haematopoietic foci, and the other was observed intravasally in the sinusoids of the liver, most probably representing primitive Kupffer cells.

Age Factors↗
PubMed1982

Ectopic germ cells: natural model for the study of germ cell sexual differentiation.

In the course of a study on the morphogenesis of the adrenal gland in random-bred Swiss albino mice, we noted the presence of ectopic germ cells in the adrenal cortexes and medullas in animals of both sexes, from day 12 1/2 of fetal development to postnatal day 12. Up to day 15 of fetal development, the cells exhibited characteristics of primordial germ cells. At day 17, and irrespective of the sex of the fetus, they all entered meiosis in synchrony with those in the ovary. Postnatally, in females as well as males, all ectopic germ cells displayed morphologic characteristics identical to those of young oocytes in unilaminar ovarian follicles. No germinal elements were seen in the adrenal glands past day 12 of life. Our study shows that mammalian germ cells are capable of undergoing sustained differentiation outside the gonads and that, in ectopic sites, they all differentiate into oocytes as they normally would in the ovary, even in males.

Adrenal Glands↗
PubMed2006

Steel factor controls midline cell death of primordial germ cells and is essential for their normal proliferation and migration.

During germ-cell migration in the mouse, the dynamics of embryo growth cause many germ cells to be left outside the range of chemoattractive signals from the gonad. At E10.5, movie analysis has shown that germ cells remaining in the midline no longer migrate directionally towards the genital ridges, but instead rapidly fragment and disappear. Extragonadal germ cell tumors of infancy, one of the most common neonatal tumors, are thought to arise from midline germ cells that failed to die. This paper addresses the mechanism of midline germ cell death in the mouse. We show that at E10.5, the rate of apoptosis is nearly four-times higher in midline germ cells than those more laterally. Gene expression profiling of purified germ cells suggests this is caused by activation of the intrinsic apoptotic pathway. We then show that germ cell apoptosis in the midline is activated by down-regulation of Steel factor (kit ligand) expression in the midline between E9.5 and E10.5. This is confirmed by the fact that removal of the intrinsic pro-apoptotic protein Bax rescues the germ-cell apoptosis seen in Steel null embryos. Two interesting things are revealed by this: first, germ-cell proliferation does not take place in these embryos after E9.0; second, migration of germ cells is highly abnormal. These data show first that changing expression of Steel factor is required for normal midline germ cell death, and second, that Steel factor is required for normal proliferation and migration of germ cells.

Animals↗
PubMed2005

Expression pattern of Bombyx vasa-like (BmVLG) protein and its implications in germ cell development.

Germ cell development in the silkworm Bombyx mori is interesting in that the species has no recognizable germ plasm, and its germ cells appear first on the ventral side of the embryo, not on the posterior pole as in Drosophila melanogaster. We previously reported the isolation of a vasa homologue (BmVLG) from B. mori and revealed the specific expression of transcript in the germ cells. In this paper, we describe the embryonic expression pattern of BmVLG protein. Consistent with the lack of recognizable germ plasm, the protein is not localized in freshly laid eggs, and its specific expression is first detectable several hours after energids penetrate the periplasm. This is in contrast to D. melanogaster, where germ cell lineage can be traced with anti-vasa antibody just after the formation of pole cells as they sequester vasa-positive germ (pole) plasm during cellularization. It is also revealed that, within the first few hours of their appearance when extensive cell movement does not seem to occur, stained cells are sometimes widely dispersed along the midline, which eventually may lead to the formation of ectopic germ cells. The implications of these results for germ cell development are discussed.

Animals↗
PubMed1998

Inhibition of genotoxic effects of mammalian germ cell mutagens.

Germ cell mutagens are among the most important chemicals for which chemopreventive agents should be sought and mechanistically defined. These mutagens may include environmental chemicals as well as drugs. In this investigation, the literature was reviewed for substances antimutagenic (or anticlastogenic) to compounds identified as mutagens in at least two germ cell studies. A complete matrix of test results was prepared to identify commonly tested pairs of germ cell mutagens and antimutagens. The categories of antimutagens most tested included vitamins, fatty acids, thiols, tannins and other phenolics. The most frequently studied mutagens were benzo[a]pyrene, cyclophosphamide, mitomycin C, and bleomycin. Based on the availability of the most relevant data, the analysis presented here focused on in vivo tests, specifically on bone marrow cytogenetics. The results indicated that antimutagens commonly found in the diet or endogenously in the body effectively antagonized the cytogenetic damage induced in the bone marrow by most of the germ cell mutagens studied to date. Bone marrow micronucleus and chromosomal aberration assays, which detect systemically active mutagens, may be predictive of similar mitigating effects in germ cells. Test results from antimutagenicity studies in germ cells, though limited, were comparable to the results from studies in the mouse bone marrow micronucleus test.

Animals↗
PubMed2006

The mouse gcd2 mutation causes primordial germ cell depletion.

Germ cell depletion 2 (gcd2) is a chemically induced recessive mutation that causes infertility in male and female mice. The infertility is caused by germ cell depletion as early as 11.5 days post-coitum, when primordial germ cells have completed their migration to the embryonic gonads. Thus, the gcd2 mutation affects the proliferation and/or survival of germ cells after they arrive in the embryonic gonad, a developmental time when little is known about the requirements for germ cell proliferation and survival. The sterility phenotype is incompletely penetrant, has variable expressivity, and is modulated by strain background. The penetrance ranges from 37% in strain C57BL/6J to nearly 100% in CAST/EiJ. Genetic mapping localized gcd2 to a approximately 1Mb region on Chr 2. This interval contains a small number of annotated genes, of which none are known to have a role in germ cell development. Sequencing the coding regions of these genes failed to reveal a mutation, and BACs containing two of the candidate genes failed to rescue the phenotype. This raises the possibilities that the gcd2 mutation resides in non-coding sequences, and regulates genes outside the genetically defined critical region.

Animals↗
PubMed1990

Interactions between somatic cells and germ cells throughout mammalian oogenesis.

Oocytes and their companion somatic cells maintain a close association throughout oogenesis and this association is essential for normal oocyte and follicular development. This review summarizes current concepts of the role of the somatic cells in the regulation of mammalian oocyte growth, the maintenance of meiotic arrest, the induction of oocyte maturation, and the acquisition of full embryonic developmental competence during oocyte maturation in vitro. Gap junctions appear to mediate these regulatory processes. The regulatory interaction of oocytes and somatic cells, however, is not unidirectional; the oocyte participates in the proliferation, development, and function of the follicular somatic cells. The oocyte secretes factors that enable the cumulus cells to synthesize hyaluronic acid and undergo cumulus expansion in response to hormonal stimulation. In addition, the oocyte produces factors that promote the proliferation of granulosa cells. These interactions in vitro do not appear to require the mediation of gap junctions. The oocyte also promotes the differentiation of granulosa cells into functional cumulus cells, but this function of the oocyte appears to require the continued presence and close association of the oocyte and granulosa cells. Therefore, oocytes and follicular somatic cells are interdependent for development and function.

Animals↗
PubMed1993

Sertoli cell and germ cell cystatin C: stage-dependent expression of two distinct messenger ribonucleic acid transcripts in rat testes.

Sertoli cells were shown to synthesize and secrete cystatin C, a potent inhibitor of cysteine proteases. The evidence for this observation was obtained from protein sequencing. Western analysis using antiserum specific to cystatin C, and immunoprecipitation of 35S protein secreted by cultured cells. The Western analysis with an antiserum to human cystatin C showed that cultured Sertoli cells secrete three previously reported immunoreactive forms of cystatin C: a predominant pair of proteins at 13-14 kDa and a less abundant 20-kDa protein. Immunohistochemical localization of cystatin C in sections of rat testes showed intense staining in Sertoli cells; no immunoreactivity was observed in spermatogonia or spermatocytes. A cDNA fragment for rat cystatin C was obtained by use of the polymerase chain reaction and was used as a probe in Northern analyses to examine the steady-state levels of cystatin C mRNA in intact testes and in Sertoli and spermatogenic cells. Sertoli cells contained a 700-nucleotide cystatin C transcript, and a mixed population of spermatids and spermatocytes contained a 550-nucleotide transcript. Analysis of RNA from purified spermatogenic cells revealed that round and condensing spermatids contained the 550-nucleotide transcript, while pachytene spermatocytes contained a smaller 500-nucleotide transcript. The 700-nucleotide transcript was present in testes isolated from rats of 5-79 days of age, the 500-nucleotide transcript was detected initially in testes from 24-day-old rats, and the 550-nucleotide transcript was detected initially at 35 days of age. Both the 500- and 550-nucleotide transcripts increased in abundance until 50 days of age. RNA from stage-synchronized testes showed that steady-state levels of both the 550- and 700-nucleotide transcripts were lowest in stages VI-VII of the cycle. These data suggest that the role of cystatin C in the testis may be to inhibit the proteolytic activity of the cysteine protease cathepsin L in all stages except stages VI-VII.

Amino Acid Sequence↗
PubMed1995

Clastogenicity of diepoxybutane in bone marrow cells and male germ cells of mice.

The bifunctional metabolite of 1,3-butadiene, 1,2:3,4-diepoxybutane (DEB), was tested in the mouse bone marrow micronucleus assay and in male mouse germ cell tests, namely the analysis of first cleavage divisions and the dominant lethal assay. All experiments were performed with single intraperitoneal treatment of the animals. In the micronucleus test, DEB doses of 4.5, 9.0, 18.0 and 36.0 mg/kg body weight were tested at a sampling interval of 24 h for bone marrow. The dose response for the induction of micronuclei in polychromatic erythrocytes was linear with the lowest effective dose of 9.0 mg/kg body weight. No sensitivity difference was observed between male and female mice. the cytogenetic analysis of first cleavage division chromosomes was performed after treatment of male mice with 17, 26, 34, 43 and 52 mg/kg body weight of DEB and mating the males to hormonally stimulated females on days 7, 14, 21 and 28 after treatment. The two higher doses caused general toxicity evidenced by the poor mating behavior of the males. Only 13 and 20% of the mated females were fertilized on day 7 after treatment of the males with 43 and 52 mg/kg body weight of DEB, respectively. An increased number of unfertilized oocytes was obtained from fertilized females on day 7 after treatment of the males with 34 mg/kg body weight of DEB. With a dose of 26 mg/kg body weight, it was demonstrated that chromosomal aberrations were only induced in spermatozoa (mating on day 7 after treatment) while spermatids (mating on days 14 and 21) and spermatocytes (mating on day 28) were not susceptible to the clastogenic effect of DEB. The response in spermatozoa in the dose range 17-34 mg/kg body weight was linear up to 26 mg/kg body weight and reached a plateau thereafter. The results of the dominant lethal experiments performed in the dose range 18-54 mg/kg body weight gave results similar to the cytogenetic study. With the highest dose tested, the toxicity and cytotoxicity during the first 8 mating days after treatment dramatically reduced the number of pregnant females and, consequently, the total implantations, so that no significant dominant lethal effect could be assessed. During mating days 9-12 (treated late spermatids), a significant dominant lethal effect was observed. With the two lower doses (18 and 36 mg/kg body weight), the dominant lethal effect was restricted to spermatozoa. The good correlation of the chromosomal aberrations with dominant lethal mutations confirms the chromosomal origin of dominant lethal effects. The clastogenic effect of DEB in somatic cells and in germ cells of mice was of the same order of magnitude.

Animals↗
PubMed1997

Risk of a second germ cell cancer after treatment of a primary germ cell cancer in 2201 Norwegian male patients.

The aim of this study was to evaluate the risk of developing a second germ cell cancer (SGCC) among male patients with a primary germ cell cancer (PGCC). SGCCs, all metachronous, developed in 60 out of 2201 males treated for a PGCC at the Norwegian Radium Hospital in Oslo from 1953 to 1990. Further, 8 patients had synchronous germ cell cancers. The relative risk (RR) of developing an SGCC was 27.6 (95% confidence interval (CI) 21.1-35.6), and the cumulative risk at 15 years of follow-up 3.9% (95% CI 2.8-5.0%). In patients with primary non-seminoma, the cumulative risk of an SGCC at 15 years of follow-up was 5.0% and in patients with primary seminoma 3.4%. Patients less than 30 years of age had a higher cumulative risk of 7.8% compared to 2.1% in older patients at 15 years of follow-up. The RR of an SGCC, however, was equal in patients with primary seminoma and in patients with primary non-seminoma. If the interval between PGCC and SGCC was < 5 years, the PGCC was most often followed by an SGCC of same histological type. Treatment applied for the PGCC did not seem to be of significant importance for the development of SGCC. In conclusion, patients with PGCC have high RR of developing an SGCC and age group < 30 years display an especially high cumulative risk.

Adult↗
PubMed1995

In-vivo genotoxicity of the alkaloid drug pilocarpine nitrate in bone marrow cells and male germ cells of mice.

Pilocarpine nitrate, an alkaloid drug of plant origin induces spindle disfunction in bone marrow cells of mice. Further studies were carried out to investigate its mutagenic effects in somatic and germ cells of mice by assessing chromosome aberrations at mitotic metaphase and as micronuclei in bone marrow cells and sperm-shape abnormality in cauda epididymides. The dose and time yield effects of the drug were investigated. The statistically significant results that were obtained for both chromosomal aberrations and micronucleus test but not for the sperm-shape abnormality test, indicated the genotoxicity of this compound in somatic cells but not in germ cells.

Animals↗
PubMed1999

mRNAs encoding a von Ebner's-like protein and the Huntington disease protein are induced in rat male germ cells by Sertoli cells.

The success of spermatogenesis is dependent upon closely coordinated interactions between Sertoli cells and germ cells. To identify specific molecules that mediate interactions between somatic cells and germ cells in the rat testis, Sertoli cell-germ cell co-cultures and mRNA differential display were used. Two cDNAs, clone 1 (660 nucleotides) and clone 2 (390 nucleotides) were up-regulated when Sertoli cells were co-cultured with pachytene spermatocytes or round spermatids. Northern blot analyses confirmed the differential display expression patterns. Sequence analyses indicated that clone 1 was similar to a von Ebner's gland protein (87% at the nucleotide level and 80% at the amino acid level) and clone 2 was identical to a region of the Huntington disease protein. The von Ebner's-like protein mRNA was induced after 4 h of co-culture, while the Huntington disease protein required 18 h of co-culture for expression. The von Ebner's-like protein was induced in germ cells by a secreted Sertoli cell factor(s) smaller than 10 kDa that is sensitive to freezing and thawing or boiling. The Huntington disease protein was induced in germ cells by a Sertoli cell secreted factor(s) larger than 10 kDa which survives freezing and thawing, but is inactivated by boiling.

Amino Acid Sequence↗
PubMed2005

Human endogenous retrovirus rec interferes with germ cell development in mice and may cause carcinoma in situ, the predecessor lesion of germ cell tumors.

Germ cell tumors (GCTs) are among the most common malignancies in young men. We have previously documented that patients with GCT frequently produce serum antibodies directed against proteins encoded by human endogenous retrovirus (HERV) type K sequences. Transcripts originating from the env gene of HERV-K, including the rec-relative of human immunodeficiency virus rev, are highly expressed in GCTs. We report here that mice that inducibly express HERV-K rec show a disturbed germ cell development and may exhibit, by 19 months of age, changes reminiscent of carcinoma in situ, the predecessor lesion of classic seminoma in humans. This provides the first direct evidence that the expression of a human endogenous retroviral gene previously established as a marker in human germ cell tumors may contribute to organ-specific tumorigenesis in a transgenic mouse model.

Alternative Splicing↗