scholarly journals Germ Cell Determinant Transmission, Segregation, and Function in the Zebrafish Embryo

Author(s):  
Celeste Eno ◽  
Francisco Pelegri

1917 ◽  
Vol s2-62 (247) ◽  
pp. 407-463
Author(s):  
J. BRONTÉ GATENBY

(1) In Smerinthus populi, Pieris brassicæ, and a number of other species of moths and butterflies the cytoplasmic bodies have been followed out. (2) The micromitosome lias been followed from the spermatocyte back into the secondary spermatogonium. It is very probably present in the primordial germ-cell. (3) The micromitosome has been definitely found in the female. (4) The micromitosome seems to divide in all divisions, and I consider that it is a constant factor in the spermatids of Smerinthus. (5) The probable nature and function of the micromitosome is discussed. (6) The mitochondria have been carefully examined in the male and female germ-cell in all stages except in the maturation division of the female and in fertilisation. (7) It has been shown that in early stages the cytoplasmic bodies of the female resemble those of the male. (8) There is a definite period, judged to be about the beginning of growth stage, when the subsequent fate of the mitochondria in the male becomes different from that of the female. (9) The remarkable formation of chromophobe and chromophile zones in the male mitochondrial body aud the use of these zones are described. (10) The formation of the macromitosome from the mitochondria is described. (11) The changes undergone by the macromitosome in sperm formation are followed out. (12) The presence of the acroblasts in the fairly early growth period of the spermatocyte is described. (13) The complicated evolutions of these bodies in division of the cells, their subsequent fate and' their probable nature are discussed. (14) The staining and fixing reactions of the cytoplasmic bodies are fully described. (15) A number of abnormalities have been described. (16) The centrosome has been shown to divide in the young spermatid, and one centrosome is probably lost, but definite evidence is not forthcoming.



Reproduction ◽  
2005 ◽  
Vol 130 (5) ◽  
pp. 627-641 ◽  
Author(s):  
K Wagoner ◽  
G Sanchez ◽  
A-N Nguyen ◽  
G C Enders ◽  
G Blanco

Two catalytic isoforms of the Na,K-ATPase, α1 and α4, are present in testis. While α1 is ubiquitously expressed in tissues, α4 predominates in male germ cells. Each isoform has distinct enzymatic properties and appears to play specific roles. To gain insight into the relevance of the Na,K-ATPase α isoforms in male germ cell biology, we have studied the expression and activity of α1 and α4 during spermatogenesis and epididymal maturation. This was explored in rat testes at different ages, in isolated spermatogenic cells and in spermatozoa from the caput and caudal regions of the epididymis. Our results show that α1 and α4 undergo differential regulation during development. Whereas α1 exhibits only modest changes, α4 increases with gamete differentiation. The most drastic changes for α4 take place in spermatocytes at the mRNA level, and with the transition of round spermatids into spermatozoa for expression and activity of the protein. No further changes are detected during transit of spermatozoa through the epididymis. In addition, the cellular distribution of α4 is modified with development, being diffusely expressed at the plasma membrane and intracellular compartments of immature cells, finally to localize to the midregion of the spermatozoon flagellum. In contrast, the α1 isoform is evenly present along the plasma membrane of the developing and mature gametes. In conclusion, the Na,K-ATPase α1 and α4 isoforms are functional in diploid, meiotic and haploid male germ cells, α4 being significantly upregulated during spermatogenesis. These results support the importance of α4 in male gamete differentiation and function.



Endocrinology ◽  
2008 ◽  
Vol 149 (10) ◽  
pp. 5035-5042 ◽  
Author(s):  
Xianpeng Sang ◽  
Matthew S. Curran ◽  
Antony W. Wood

IGF signaling has been shown to stimulate migration of multiple cell types in vitro, but few studies have confirmed an equivalent function for IGF signaling in vivo. We recently showed that suppression of IGF receptors in the zebrafish embryo disrupts primordial germ cell (PGC) migration, but the mechanism underlying these effects has not been elucidated. We hypothesized that PGCs are intrinsically dependent upon IGF signaling during the migratory phase of development. To test this hypothesis, we first examined the spatial expression patterns of IGF ligand genes (igf1, igf2a, and igf2b) in the zebrafish embryo. In situ analyses revealed distinct expression patterns for each IGF ligand gene, with igf2b mRNA expressed in a spatial pattern that correlates strongly with PGC migration. To determine whether PGC migration is responsive to IGF signaling in vivo, we synthesized gene hybrid expression constructs that permit conditional overexpression of IGF ligands by PGCs into the PGC microenvironment. Conditional overexpression of IGF ligands consistently disrupted PGC migration, confirming that PGC migration is sensitive to local aberrations in IGF signaling. Finally, we show that conditional suppression of IGF signaling, via PGC-specific overexpression of a mutant IGF-I receptor, disrupts PGC migration, confirming that zebrafish PGCs intrinsically require IGF signaling for directional migration in vivo. Collectively, these studies confirm an in vivo role for IGF signaling in cell migration and identify a candidate ligand gene (igf2b) regulating PGC migration in the zebrafish.



BMC Cancer ◽  
2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Ildar V. Gainetdinov ◽  
Yulia V. Skvortsova ◽  
Sofia A. Kondratieva ◽  
Alexey Klimov ◽  
Alexey A. Tryakin ◽  
...  


1996 ◽  
Vol 5 (2) ◽  
pp. 65-71 ◽  
Author(s):  
Eli Y Adashi ◽  
Richard M Rohan

Ovarian folliculogenesis is an exponential process marked by dramatic proliferation and differentiation of the somatic and germ cell elements of the follicle. Although the central roles of gonadotropins and of gonadal steroids in this explosive agenda are well accepted, the variable fate of follicles afforded comparable gonadotropic stimulation suggests the existence of additional intraovarian modulatory systems. Accordingly, consideration must be given to another set (or sets) of regulatory principles that may provide these missing modulatory loops. The work of multiple contributors favors the hypothesis that these modulatory loops are comprised of a host of peptidergic principles which engage in situ in the modulation of ovarian growth and function. In its capacity as an intraovarian regulator, a given agent may be acting independently of, as an amplifier of, as an attenuator of, or even as a mediator of, gonadotropin action. Together, gonadotropins, steroids, and locally derived peptidergic principles form a triad that modulates the growth and differentiation of ovarian follicles (Figure 1).



2015 ◽  
Vol 26 (22) ◽  
pp. 4015-4032 ◽  
Author(s):  
Catherine E. Au ◽  
Louis Hermo ◽  
Elliot Byrne ◽  
Jeffrey Smirle ◽  
Ali Fazel ◽  
...  

The molecular basis of changes in structure, cellular location, and function of the Golgi apparatus during male germ cell differentiation is unknown. To deduce cognate Golgi proteins, we isolated germ cell Golgi fractions, and 1318 proteins were characterized, with 20 localized in situ. The most abundant protein, GL54D of unknown function, is characterized as a germ cell–specific Golgi-localized type II integral membrane glycoprotein. TM9SF3, also of unknown function, was revealed to be a universal Golgi marker for both somatic and germ cells. During acrosome formation, several Golgi proteins (GBF1, GPP34, GRASP55) localize to both the acrosome and Golgi, while GL54D, TM9SF3, and the Golgi trafficking protein TMED7/p27 are segregated from the acrosome. After acrosome formation, GL54D, TM9SF3, TMED4/p25, and TMED7/p27 continue to mark Golgi identity as it migrates away from the acrosome, while the others (GBF1, GPP34, GRASP55) remain in the acrosome and are progressively lost in later steps of differentiation. Cytoplasmic HSP70.2 and the endoplasmic reticulum luminal protein-folding enzyme PDILT are also Golgi recruited but only during acrosome formation. This resource identifies abundant Golgi proteins that are expressed differentially during mitosis, meiosis, and postacrosome Golgi migration, including the last step of differentiation.



2009 ◽  
Vol 42 (4) ◽  
pp. 291-303 ◽  
Author(s):  
M H Abel ◽  
D Baban ◽  
S Lee ◽  
H M Charlton ◽  
P J O'Shaughnessy

FSH acts through the Sertoli cell to ensure normal testicular development and function. To identify transcriptional mechanisms through which FSH acts in the testis, we have treated gonadotrophin-deficient hypogonadal (hpg) mice with recombinant FSH and measured changes in testicular transcript levels using microarrays and real-time PCR 12, 24 and 72 h after the start of treatment. Approximately 400 transcripts were significantly altered at each time point by FSH treatment. At 12 h, there was a clear increase in the levels of a number of known Sertoli cell transcripts (e.g. Fabp5, Lgals1, Tesc, Scara5, Aqp5). Additionally, levels of Leydig cell transcripts were also markedly increased (e.g. Ren1, Cyp17a1, Akr1b7, Star, Nr4a1). This was associated with a small but significant rise in testosterone at 24 and 72 h. At 24 h, androgen-dependent Sertoli cell transcripts were up-regulated (e.g. Rhox5, Drd4, Spinlw1, Tubb3 and Tsx) and this trend continued up to 72 h. By contrast with the somatic cells, only five germ cell transcripts (Dkkl1, Hdc, Pou5f1, Zfp541 and 1700021K02Rik) were altered by FSH within the time-course of the experiment. Analysis of canonical pathways showed that FSH induced a general decline in transcripts related to formation and regulation of tight junctions. Results show that FSH acts directly and indirectly to induce rapid changes in Sertoli cell and Leydig cell transcript levels in the hpg mouse but that effects on germ cell development must occur over a longer time-span.



2007 ◽  
Vol 213 (1) ◽  
pp. 72-81 ◽  
Author(s):  
S Schweyer ◽  
A Bachem ◽  
F Bremmer ◽  
HJ Steinfelder ◽  
A Soruri ◽  
...  


Zygote ◽  
2007 ◽  
Vol 15 (2) ◽  
pp. 117-128 ◽  
Author(s):  
S. Kageyama ◽  
W. Gunji ◽  
M. Nakasato ◽  
Y. Murakami ◽  
M. Nagata ◽  
...  

SummaryThe transition from a differentiated germ cell into a totipotent zygote during oogenesis and preimplantation development is critical to the creation of a new organism. During this period, cell characteristics change dynamically, suggesting that a global alteration of gene expression patterns occurs, which is regulated by global changes in various epigenetic factors. Among these, transcription factors (TFs) are essential in the direct regulation of transcription and also play important roles in determining cell characteristics. However, no comprehensive analysis of TFs from germ cells to embryos had been undertaken. We used mRNA amplification systems and microarrays to conduct a genomewide analysis of TFs at various stages of oogenesis and preimplantation development. The greatest alteration in TFs occurred between the 1- and 2-cell stages, at which time zygotic genome activation (ZGA) occurs. Our analysis of TFs classified by structure and function revealed several specific patterns of change. Basic transcription factors, which are the general components of transcription, increased transiently at the 2-cell stage, while homeodomain (HD) TFs were expressed specifically in the oocyte. TFs containing the Rel homology region (RHR) and Ets domains were expressed at a high level in 2-cell and blastocyst embryos. Thus, the global TF dynamics that occur during oogenesis and preimplantation development seem to regulate the transition from germ-cell-type to embryo-type gene expression.



2015 ◽  
Vol 26 (9) ◽  
pp. 1752-1763 ◽  
Author(s):  
Michael J. W. VanGompel ◽  
Ken C. Q. Nguyen ◽  
David H. Hall ◽  
William T. Dauer ◽  
Lesilee S. Rose

Torsin proteins are AAA+ ATPases that localize to the endoplasmic reticular/nuclear envelope (ER/NE) lumen. A mutation that markedly impairs torsinA function causes the CNS disorder DYT1 dystonia. Abnormalities of NE membranes have been linked to torsinA loss of function and the pathogenesis of DYT1 dystonia, leading us to investigate the role of the Caenorhabditis elegans torsinA homologue OOC-5 at the NE. We report a novel role for torsin in nuclear pore biology. In ooc-5–mutant germ cell nuclei, nucleoporins (Nups) were mislocalized in large plaques beginning at meiotic entry and persisted throughout meiosis. Moreover, the KASH protein ZYG-12 was mislocalized in ooc-5 gonads. Nups were mislocalized in adult intestinal nuclei and in embryos from mutant mothers. EM analysis revealed vesicle-like structures in the perinuclear space of intestinal and germ cell nuclei, similar to defects reported in torsin-mutant flies and mice. Consistent with a functional disruption of Nups, ooc-5–mutant embryos displayed impaired nuclear import kinetics, although the nuclear pore-size exclusion barrier was maintained. Our data are the first to demonstrate a requirement for a torsin for normal Nup localization and function and suggest that these functions are likely conserved.



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