Behaviour of germ cells and sexual differentiation in late embryonic and early postnatal mouse chimeras

Development ◽  
1970 ◽  
Vol 23 (2) ◽  
pp. 395-405
Author(s):  
Ewa T. Mystkowska ◽  
Andrzej K. Tarkowski
Keyword(s):  
Environmental Factors ◽  
Germ Cells ◽  
Sexual Differentiation ◽  
Genetic Factors ◽  
Sex Chromosome ◽  
Primordial Germ Cells ◽  
Adult Males ◽  
Genetic Types ◽  
Mouse Chimeras

The purpose of the present study was to trace the fate of primordial germ cells in mouse chimeras of XX/XY constitution. In this type of research one hopes to obtain knowledge of the role of intrinsic genetic factors and of environmental factors (the environment provided by the gonads) in initiating and directing the course of gametogenesis in mammals. Data obtained up to the present show that adult males with sex chromosome chimerism produce spermatozoa only from the genetically male component and that in these individuals XX germ cells are not present among primary spermatocytes in diakinesis (Mystkowska & Tarkowski, 1968). The first of these observations has recently been confirmed by Mintz (1968). Since chimeras formed of components of the same genetic sex can produce gametes of both ‘parental’ genetic types, it seems likely that, in XX/XY individuals also, primordial germ cells of both types are formed and populate the genital ridges, and that the absence of XX germ cells in adult XX/XY males is secondary rather than primary.

scholarly journals Retinoic Acid and Germ Cell Development in the Ovary and Testis

Biomolecules ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 775 ◽  
Author(s):  
Tsutomu Endo ◽  
Maria M. Mikedis ◽  
Peter K. Nicholls ◽  
David C. Page ◽  
Dirk G. de Rooij
Keyword(s):  
Retinoic Acid ◽  
Germ Cells ◽  
Sexual Differentiation ◽  
Fetal Development ◽  
Primordial Germ Cells ◽  
Male Germ Cells ◽  
Developmental Transitions ◽  
Cycle Arrest ◽  
Meiotic Initiation

Retinoic acid (RA), a derivative of vitamin A, is critical for the production of oocytes and sperm in mammals. These gametes derive from primordial germ cells, which colonize the nascent gonad, and later undertake sexual differentiation to produce oocytes or sperm. During fetal development, germ cells in the ovary initiate meiosis in response to RA, whereas those in the testis do not yet initiate meiosis, as they are insulated from RA, and undergo cell cycle arrest. After birth, male germ cells resume proliferation and undergo a transition to spermatogonia, which are destined to develop into haploid spermatozoa via spermatogenesis. Recent findings indicate that RA levels change periodically in adult testes to direct not only meiotic initiation, but also other key developmental transitions to ensure that spermatogenesis is precisely organized for the prodigious output of sperm. This review focuses on how female and male germ cells develop in the ovary and testis, respectively, and the role of RA in this process.

scholarly journals Absence of X-chromosome dosage compensation in the primordial germ cells of Drosophila embryos

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryoma Ota ◽  
Makoto Hayashi ◽  
Shumpei Morita ◽  
Hiroki Miura ◽  
Satoru Kobayashi
Keyword(s):  
X Chromosome ◽  
Germ Cells ◽  
Dosage Compensation ◽  
Sex Chromosome ◽  
Primordial Germ Cells ◽  
Histone H4 ◽  
X Chromosomes ◽  
Essential Components ◽  
Msl Complex ◽  
Male Specific

AbstractDosage compensation is a mechanism that equalizes sex chromosome gene expression between the sexes. In Drosophila, individuals with two X chromosomes (XX) become female, whereas males have one X chromosome (XY). In males, dosage compensation of the X chromosome in the soma is achieved by five proteins and two non-coding RNAs, which assemble into the male-specific lethal (MSL) complex to upregulate X-linked genes twofold. By contrast, it remains unclear whether dosage compensation occurs in the germline. To address this issue, we performed transcriptome analysis of male and female primordial germ cells (PGCs). We found that the expression levels of X-linked genes were approximately twofold higher in female PGCs than in male PGCs. Acetylation of lysine residue 16 on histone H4 (H4K16ac), which is catalyzed by the MSL complex, was undetectable in these cells. In male PGCs, hyperactivation of X-linked genes and H4K16ac were induced by overexpression of the essential components of the MSL complex, which were expressed at very low levels in PGCs. Together, these findings indicate that failure of MSL complex formation results in the absence of X-chromosome dosage compensation in male PGCs.

On the role of germ cells in planarian regeneration

Development ◽  
1980 ◽  
Vol 55 (1) ◽  
pp. 53-63
Author(s):  
V. Gremigni ◽  
C. Miceli ◽  
I. Puccinelli
Keyword(s):  
Chromosome Number ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Karyological Analysis ◽  
Blastema Formation ◽  
Planarian Regeneration ◽  
Somatic Tissues ◽  
Caudal Area ◽  
Complete Regeneration

Specimens from a polyploid biotype of Dugesia lugubris s.l. were used to clarify the role and fate of germ cells during planarian regeneration. These specimens provide a useful karyological marker because embryonic and somatic cells (3n = 12) can be easily distinguished from male (2n = 8) and female (6n = 24) germ cells by their chromosome number. We succeed in demonstrating how primordial germ cells participate in blastema formation and take part in rebuilding somatic tissues. This evidence was obtained by cutting each planarian specimen twice at appropriate levels. The first aimed to induce primordial germ cells to migrate to the wound. The second cut was performed after complete regeneration and aimed to obtain a blastema from a cephalic or caudal area devoid of gonads. A karyological analysis of mitotic cells present in each blastema obtained after the second cut provided evidence that cells, originally belonging to the germ lines, are still present in somatic tissues even months after complete regeneration. The role of primordial germ cells in planarian regeneration was finally discussed in relation to the phenomenon of metaplasia or transdifferentiation.

Dual role of Ovol2 on the germ cell lineage segregation during gastrulation in mouse embryogenesis

Development ◽  
2022 ◽  
Author(s):  
Yuki Naitou ◽  
Go Nagamatsu ◽  
Nobuhiko Hamazaki ◽  
Kenjiro Shirane ◽  
Masafumi Hayashi ◽  
...  
Keyword(s):  
Germ Cells ◽  
Splice Variant ◽  
Epithelial To Mesenchymal Transition ◽  
Functional Relationship ◽  
Germ Line ◽  
Primordial Germ Cells ◽  
Cell Lineage ◽  
Animal Kingdom ◽  
Mesenchymal Transition

In mammals, primordial germ cells (PGCs), the origin of the germ line, are specified from the epiblast at the posterior region where gastrulation simultaneously occurs, yet the functional relationship between PGC specification and gastrulation remains unclear. Here, we show that Ovol2, a transcription factor conserved across the animal kingdom, balances these major developmental processes by repressing the epithelial-to-mesenchymal transition (EMT) driving gastrulation and the upregulation of genes associated with PGC specification. Ovol2a, a splice variant encoding a repressor domain, directly regulates EMT-related genes and consequently induces re-acquisition of potential pluripotency during PGC specification, whereas Ovol2b, another splice variant missing the repressor domain, directly upregulates genes associated with PGC specification. Taken together, these results elucidate the molecular mechanism underlying allocation of the germ line among epiblast cells differentiating into somatic cells through gastrulation.

Functional requirement of gp130-mediated signaling for growth and survival of mouse primordial germ cells in vitro and derivation of embryonic germ (EG) cells

Development ◽  
1996 ◽  
Vol 122 (4) ◽  
pp. 1235-1242 ◽  
Author(s):  
U. Koshimizu ◽  
T. Taga ◽  
M. Watanabe ◽  
M. Saito ◽  
Y. Shirayoshi ◽  
...  
Keyword(s):  
Germ Cells ◽  
Intracellular Signaling ◽  
Primordial Germ Cells ◽  
Cell Formation ◽  
Embryonic Stem ◽  
Oncostatin M ◽  
Receptor Complexes ◽  
Binding Subunit

Leukemia inhibitory factor (LIF) is a cytokine known to influence proliferation and/or survival of mouse primordial germ cells (PGC) in culture. The receptor complex for LIF comprises LIF-binding subunit and non-binding signal transducer, gp130. The gp130 was originally identified as a signal-transducing subunit of interleukin (IL)-6 and later also found to be a functional component of receptor complexes for other LIF-related cytokines (oncostatin M [OSM], ciliary neurotrophic factor [CNTF] and IL-11). In this study, we have analyzed the functional role of gp130-mediated signaling in PGC growth in vitro. OSM was able to fully substitute for LIF; both cytokines promoted the proliferation of migratory PGC (mPGC) and enhanced the viability of postmigratory (colonizing) PGC (cPGC) when cultured on SI/SI4-m220 cells. Interestingly, IL-11 stimulated mPGC growth comparable to LIF and OSM, but did not affect cPGC survival. IL-6 and CNTF did not affect PGC. In addition, a combination of IL-6 and soluble IL-6 binding subunit (sIL-6R), which is known to activate intracellular signaling via gp130, fully reproduced the LIF action of PGC. Both in the presence and absence of LIF, addition of neutralizing antibody against gp130 in culture remarkably blocked cPGC survival. These results suggest a pivotal role of gp130 in PGC development, especially that it is indispensable for cPGC survival as comparable to the c-KIT-mediated action. We have further demonstrated that a combination of LIF with forskolin or retinoic acid, a potent mitogen for PGC, supported the proliferation of PGC, leading to propagation of the embryonic stem cell-like cells, termed embryonic germ (EG) cells. Since EG cells were also obtained by using OSM or the IL-6/sIL-6R complex in place of LIF, a significant contribution of gp130-mediated signaling in EG cell formation was further suggested.

Effects of ten–eleven translocation 1 (Tet1) on DNA methylation and gene expression in chicken primordial germ cells

2019 ◽  
Vol 31 (3) ◽  
pp. 509 ◽  
Author(s):  
Minli Yu ◽  
Dongfeng Li ◽  
Wanyan Cao ◽  
Xiaolu Chen ◽  
Wenxing Du
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Germ Cells ◽  
Dna Methyltransferase ◽  
Primordial Germ Cells ◽  
Dna Demethylation ◽  
Caveolin 1 ◽  
Expression Of Genes ◽  
Deleted In Azoospermia

Ten–eleven translocation 1 (Tet1) is involved in DNA demethylation in primordial germ cells (PGCs); however, the precise regulatory mechanism remains unclear. In the present study the dynamics of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) in developing PGCs and the role of Tet1 in PGC demethylation were analysed. Results show that 5mC levels dropped significantly after embryonic Day 4 (E4) and 5hmC levels increased reaching a peak at E5–E5.5. Interestingly, TET1 protein was highly expressed during E5 to E5.5, which showed a consistent trend with 5hmC. The expression of pluripotency-associated genes (Nanog, PouV and SRY-box 2 (Sox2)) and germ cell-specific genes (caveolin 1 (Cav1), piwi-like RNA-mediated gene silencing 1 (Piwi1) and deleted in azoospermia-like (Dazl)) was upregulated after E5, whereas the expression of genes from the DNA methyltransferase family was decreased. Moreover, the Dazl gene was highly methylated in early PGCs and then gradually hypomethylated. Knockdown of Tet1 showed impaired survival and proliferation of PGCs, as well as increased 5mC levels and reduced 5hmC levels. Further analysis showed that knockdown of Tet1 led to elevated DNA methylation levels of Dazl and downregulated gene expression including Dazl. Thus, this study reveals the dynamic epigenetic reprogramming of chicken PGCs invivo and the molecular mechanism of Tet1 in regulating genomic DNA demethylation and hypomethylation of Dazl during PGC development.

Role of stem cell factor in somatic–germ cell interactions during prenatal oogenesis

Zygote ◽  
1996 ◽  
Vol 4 (04) ◽  
pp. 349-351 ◽  
Author(s):  
Massimo De Felici ◽  
Anna Di Carlo ◽  
Maurizio Pesce
Keyword(s):  
Stem Cell ◽  
Germ Cells ◽  
Stem Cell Factor ◽  
Molecular Mechanisms ◽  
Primordial Germ Cells ◽  
Significant Progress ◽  
Proliferation And Differentiation ◽  
Complex Events ◽  
Mechanisms Of Migration

During embryogenesis germ cells originate from primordial germ cells (PGCs). The development of mammalian PGCs involves a number of complex events (formation and segregation of PGC precursors, PGC migration and proliferation) which lead to the differentiation of oocytes or prospermatogonia (for a review see De Feliciet al., 1992). During recent years developments in methods for isolation, purification and culture of mouse PGCs have led to significant progress in the understanding of molecular mechanisms of migration, proliferation and differentiation of these cells (for reviews see De Felici, 1994; and De Felici & Pesce, 1994a). In this paper we describe the key role played by stem cell factor (SCF) in PGC development and early folliculogenesis.

scholarly journals Small non-coding RNA profiling and the role of piRNA pathway genes in the protection of chicken primordial germ cells

BMC Genomics ◽  
2014 ◽  
Vol 15 (1) ◽  
pp. 757 ◽  
Author(s):  
Deivendran Rengaraj ◽  
Sang Lee ◽  
Tae Park ◽  
Hong Lee ◽  
Young Kim ◽  
...  
Keyword(s):  
Germ Cells ◽  
Primordial Germ Cells ◽  
Rna Profiling ◽  
Non Coding Rna ◽  
Pirna Pathway

A Behavioral-Genetic Analysis of Health Anxiety: Implications for the Cognitive-Behavioral Model of Hypochondriasis

2008 ◽  
Vol 22 (2) ◽  
pp. 143-153 ◽  
Author(s):  
Steven Taylor ◽  
Kerry L. Jang ◽  
Murray B. Stein ◽  
Gordon J. G. Asmundson
Keyword(s):  
Environmental Factors ◽  
Genetic Factors ◽  
Health Anxiety ◽  
Environmental Influences ◽  
Behavioral Model ◽  
Cognitive Behavioral ◽  
Data Set ◽  
University Of British Columbia ◽  
Cognitive Behavioral Model

The leading contemporary cognitive-behavioral model of excessive health anxiety (HA) emphasizes the importance of environmental factors, such as learning experiences. The model has little to say about the role of genetic factors and, by ignoring these factors, seems to imply that they are unimportant. In contrast, results from the University of British Columbia Twin Study, using a sample of 88 monozygotic and 65 dizygotic twin pairs, indicated that various facets of HA, such as excessive disease fear, unrealistic beliefs that one has a serious disease, and HA-related interference in functioning, are moderately heritable. The present study extended the analyses of this data set by investigating the extent to which the various facets of HA are due to genetic or environmental factors that are common to all facets versus specific to each facet. Results indicated that all facets of HA are influenced by a common set of genes—there was very little evidence of facet-specific genetic influences. There was considerably stronger evidence for facet-specific environmental influences, where each facet is strongly influenced by environmental experiences that are specific to that facet. However, there was also evidence that particular environmental influences—especially those that shape disease conviction—also influence some of the other HA facets (fear and interference). The importance of environmental factors is consistent with the cognitive-behavioral model of HA, although the model needs to be refined to account for the role of genetic factors. Possibilities for refining the model are discussed, along with promising research directions to better understand the role of genes and the environment in HA.

scholarly journals The Differential Role of Human Cationic Trypsinogen (PRSS1) p.R122H Mutation in Hereditary and Nonhereditary Chronic Pancreatitis: A Systematic Review and Meta-Analysis

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Cheng Hu ◽  
Li Wen ◽  
Lihui Deng ◽  
Chenlong Zhang ◽  
Aurelia Lugea ◽  
...  
Keyword(s):  
Systematic Review ◽  
Chronic Pancreatitis ◽  
Environmental Factors ◽  
Genetic Factors ◽  
Meta Analysis ◽  
Case Control Studies ◽  
Complex Disorder ◽  
Increased Risk ◽  
Cationic Trypsinogen

Background. Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). ThePRSS1p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations ofPRSS1p.R122H mutation with CP of diverse etiology.Methods. The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP.Results. A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall,PRSS1p.R122H mutation was significantly associated with an increased risk of CP (OR = 4.78[1.13–20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (OR = 65.52[9.09–472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP.Conclusions. Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors.

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