Evaluation of degenerating germ cells in normal juvenile mice

Genome ◽  
2009 ◽  
Vol 52 (10) ◽  
pp. 891-896 ◽  
Author(s):  
Anastassia Trifonova ◽  
Peter B. Moens
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Germ Cells ◽  
Normal Component ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Electron Microscopic ◽  
Cell Degeneration ◽  
Novel Approach ◽  
Two Generations ◽  
Germ Cell Degeneration

Absence of spermiogenesis in mice with meiotic defects complicates the staging of meiotic arrest using light microscopy. Consequently, new methodologies are required to establish accurate relationships among germ cells. In this study, we utilized a novel approach to analyze germ cell degeneration in juvenile mice. We used terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) in combination with meiosis-specific antibodies. Germ cell degeneration is a normal component of early spermatogenesis in juvenile mice. The incidence of germ cell death was monitored at various postnatal ages of mice using the TUNEL assay to quantify the incidence of apoptosis. Cell death occurred predominantly at 15.5 days after birth. It was found that groups of apoptotic cells were apparent in tubules containing two generations of spermatocytes that form in two progressive cohorts. Electron microscopic observations further illustrated that the majority of cells in the first cohort are in late pachytene, while groups of cells in the second cohort can degenerate in early pachytene. The methodology utilized in this study is significant because it allows one to accurately determine the point at which germ cells arrest. Consequently, we believe that these methods can be applied to study animals with meiotic defects that prevent spermiogenesis.

Bone morphogenetic protein 8A plays a role in the maintenance of spermatogenesis and the integrity of the epididymis

Development ◽  
1998 ◽  
Vol 125 (6) ◽  
pp. 1103-1112 ◽  
Author(s):  
G.Q. Zhao ◽  
L. Liaw ◽  
B.L. Hogan
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Targeted Mutagenesis ◽  
Chromosome 4 ◽  
Female Reproduction ◽  
Cell Degeneration ◽  
Male Germ Cells ◽  
Morphogenetic Protein ◽  
Germ Cell Degeneration

The murine Bmp8a and Bmp8b genes are tightly linked on mouse chromosome 4 and have similar expression during reproduction. Previous studies have shown that targeted mutagenesis of Bmp8b causes male infertility due to germ cell degeneration. To investigate the function of Bmp8a, we have inactivated the gene by homologous recombination. Heterozygous and homozygous Bmp8a mutants reveal normal embryonic and postnatal development. Despite high levels of Bmp8a expression in the deciduum, homozygous mutant females have normal fertility, suggesting that the gene is not essential for female reproduction. Bmp8a and Bmp8b are expressed in similar patterns in male germ cells. Unlike homozygous Bmp8btm1 mutants, homozygous Bmp8atm1 males do not show obvious germ cell defects during the initiation of spermatogenesis. However, germ cell degeneration is observed in 47% of adult homozygous Bmp8atm1 males, establishing a role of Bmp8a in the maintenance of spermatogenesis. A small proportion of the mating homozygous Bmp8atm1 males also show degeneration of the epididymal epithelium, indicating a novel role for BMPs in the control of epididymal function.

STUDIES ON ARTIFICIAL CRYPTORCHIDISM: DEGENERATIVE AND REGENERATIVE CHANGES IN THE GERMINAL EPITHELIUM OF THE RAT TESTIS

1963 ◽  
Vol 27 (2) ◽  
pp. 241-251 ◽  
Author(s):  
E. J. CLEGG
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Initial Phase ◽  
Environmental Temperature ◽  
Degenerative Changes ◽  
Germinal Epithelium ◽  
Seminiferous Tubules ◽  
Cell Degeneration ◽  
Rat Testis ◽  
Germ Cell Degeneration

SUMMARY 1. In the rat bilateral artificial cryptorchidism results in degenerative changes in the seminiferous tubules which are maximal about the 15th day after operation. Up to this stage all germ cells are reduced in number, spermatogonia being least affected and spermatids most. Spermatogonial mitoses and spermatocytial meioses are also inhibited to some extent. 2. Following this initial phase of degeneration there is a partial regeneration, most marked in the case of spermatocytes and total germ cells, which at the 35th day results in the formation of early spermatids. 3. The degree of germ-cell degeneration after 15 days of cryptorchidism is greater than the maximal degeneration after hypophysectomy. It is considered that the increased environmental temperature of the testes may 'block' the action of gonadotrophins on the seminiferous tubules as well as damage the germ cells directly. The occurrence of a certain degree of regeneration may indicate that this 'block' can be overcome to some extent by increased production of pituitary gonadotrophins.

scholarly journals The developing ovary of the South American plains vizcacha, Lagostomus maximus (Mammalia, Rodentia): massive proliferation with no sign of apoptosis-mediated germ cell attrition

Reproduction ◽  
2011 ◽  
Vol 141 (5) ◽  
pp. 633-641 ◽  
Author(s):  
N P Leopardo ◽  
F Jensen ◽  
M A Willis ◽  
M B Espinosa ◽  
A D Vitullo
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Ovarian Tissue ◽  
Tunel Assay ◽  
South American ◽  
Follicular Atresia ◽  
The South ◽  
Cell Degeneration ◽  
Lagostomus Maximus ◽  
Apoptotic Activity

Apoptosis-dependent massive germ cell death is considered a constitutive trait of the developing mammalian ovary that eliminates 65–85% of the germinal tissue depending on the species. After birth and during adult lifetime, apoptotic activity moves from the germ cell proper to the somatic compartment, decimating germ cells through follicular atresia until the oocyte reserve is exhausted. In contrast, the South American rodent Lagostomus maximus shows suppressed apoptosis-dependent follicular atresia in the adult ovary, with continuous folliculogenesis and massive polyovulation, which finally exhausts the oocyte pool. The absence of follicular atresia in adult L. maximus might arise from a failure to move apoptosis from the germinal stratum to the somatic compartment after birth or being a constitutive trait of the ovarian tissue with no massive germ cell degeneration in the developing ovary. We tested these possibilities by analysing oogenesis, expression of germ cell-specific VASA protein, apoptotic proteins BCL2 and BAX, and DNA fragmentation by TUNEL assay in the developing ovary of L. maximus. Immunolabelling for VASA revealed a massive and widespread colonisation of the ovary and proliferation of germ cells organised in nests that disappeared at late development when folliculogenesis began. No sign of germ cell attrition was found at any time point. BCL2 remained positive throughout oogenesis, whereas BAX was slightly detected in early development. TUNEL assay was conspicuously negative throughout the development. These results advocate for an unrestricted proliferation of germ cells, without apoptosis-driven elimination, as a constitutive trait of L. maximus ovary as opposed to what is normally found in the developing mammalian ovary.

scholarly journals Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1011-1022 ◽  
Author(s):  
T.L. Gumienny ◽  
E. Lambie ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
M.O. Hengartner
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Somatic Cell ◽  
Cell Fate ◽  
Germ Cells ◽  
Mapk Pathway ◽  
Apoptotic Cell ◽  
C Elegans ◽  
Pathway Activation

Development of the nematode Caenorhabditis elegans is highly reproducible and the fate of every somatic cell has been reported. We describe here a previously uncharacterized cell fate in C. elegans: we show that germ cells, which in hermaphrodites can differentiate into sperm and oocytes, also undergo apoptotic cell death. In adult hermaphrodites, over 300 germ cells die, using the same apoptotic execution machinery (ced-3, ced-4 and ced-9) as the previously described 131 somatic cell deaths. However, this machinery is activated by a distinct pathway, as loss of egl-1 function, which inhibits somatic cell death, does not affect germ cell apoptosis. Germ cell death requires ras/MAPK pathway activation and is used to maintain germline homeostasis. We suggest that apoptosis eliminates excess germ cells that acted as nurse cells to provide cytoplasmic components to maturing oocytes.

scholarly journals Germ cell connectivity enhances cell death in response to DNA damage in the Drosophila testis

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Kevin L Lu ◽  
Yukiko M Yamashita
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Germ Cell ◽  
Germ Cells ◽  
High Sensitivity ◽  
Next Generation ◽  
Drosophila Testis

Two broadly known characteristics of germ cells in many organisms are their development as a ‘cyst’ of interconnected cells and their high sensitivity to DNA damage. Here we provide evidence that in the Drosophila testis, connectivity serves as a mechanism that confers to spermatogonia a high sensitivity to DNA damage. We show that all spermatogonia within a cyst die synchronously even when only a subset of them exhibit detectable DNA damage. Mutants of the fusome, an organelle that is known to facilitate intracyst communication, compromise synchronous spermatogonial death and reduces overall germ cell death. Our data indicate that a death-promoting signal is shared within the cyst, leading to death of the entire cyst. Taken together, we propose that intercellular connectivity supported by the fusome uniquely increases the sensitivity of the germline to DNA damage, thereby protecting the integrity of gamete genomes that are passed on to the next generation.

scholarly journals Overexpression of peroxisomal testis-specific 1 protein induces germ cell apoptosis and leads to infertility in male mice

2011 ◽  
Vol 22 (10) ◽  
pp. 1766-1779 ◽  
Author(s):  
Karina Kaczmarek ◽  
Maja Studencka ◽  
Andreas Meinhardt ◽  
Krzysztof Wieczerzak ◽  
Sven Thoms ◽  
...  
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Germ Cells ◽  
Specific Gene ◽  
Male Mice ◽  
Terminal Part ◽  
Male Germ Cells ◽  
Germ Cell Apoptosis ◽  
Induced Apoptosis

 Peroxisomal testis-specific 1 gene (Pxt1) is the only male germ cell–specific gene that encodes a peroxisomal protein known to date. To elucidate the role of Pxt1 in spermatogenesis, we generated transgenic mice expressing a c-MYC-PXT1 fusion protein under the control of the PGK2 promoter. Overexpression of Pxt1 resulted in induction of male germ cells’ apoptosis mainly in primary spermatocytes, finally leading to male infertility. This prompted us to analyze the proapoptotic character of mouse PXT1, which harbors a BH3-like domain in the N-terminal part. In different cell lines, the overexpression of PXT1 also resulted in a dramatic increase of apoptosis, whereas the deletion of the BH3-like domain significantly reduced cell death events, thereby confirming that the domain is functional and essential for the proapoptotic activity of PXT1. Moreover, we demonstrated that PXT1 interacts with apoptosis regulator BAT3, which, if overexpressed, can protect cells from the PXT1-induced apoptosis. The PXT1-BAT3 association leads to PXT1 relocation from the cytoplasm to the nucleus. In summary, we demonstrated that PXT1 induces apoptosis via the BH3-like domain and that this process is inhibited by BAT3.

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