scholarly journals Germ Cell Loss Induced by 12C6+ Ion Irradiation in Young Female Mice

2006 ◽  
Vol 47 (2) ◽  
pp. 131-134 ◽  
Author(s):  
Hong ZHANG ◽  
Xu ZHANG ◽  
Zhigang YUAN ◽  
Xiaoda LI ◽  
Wenjian LI ◽  
...  
Keyword(s):  
Germ Cell ◽  
Ion Irradiation ◽  
Cell Loss ◽  
Young Female ◽  
Female Mice

scholarly journals PUMA regulates germ cell loss and primordial follicle endowment in mice

Reproduction ◽  
2014 ◽  
Vol 148 (2) ◽  
pp. 211-219 ◽  
Author(s):  
Michelle Myers ◽  
F Hamish Morgan ◽  
Seng H Liew ◽  
Nadeen Zerafa ◽  
Thilini Upeksha Gamage ◽  
...  
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Germ Cells ◽  
Ovarian Development ◽  
Fold Increase ◽  
Cell Loss ◽  
Postnatal Life ◽  
Critical Determinant ◽  
Primordial Follicles ◽  
Female Mice

The number of primordial follicles initially established within the ovary is influenced by the extent of germ cell death during foetal ovarian development, but the mechanisms that mediate this death have not been fully uncovered. In this study, we identified BBC3 (PUMA) (p53 upregulated modulator of apoptosis, also known as BCL2-binding component 3), a pro-apoptotic BH3-only protein belonging to the BCL2 family, as a critical determinant of the number of germ cells during ovarian development. Targeted disruption of the Bbc3 gene revealed a significant increase in the number of germ cells as early as embryonic day 13.5. The number of germ cells remained elevated in Bbc3−/− female mice compared with WT female mice throughout the remainder of embryonic and early postnatal life, resulting in a 1.9-fold increase in the number of primordial follicles in the ovary on postnatal day 10. The increase in the number of germ cells observed in the ovaries of Bbc3−/− mice could not be attributed to the altered proliferative activity of germ cells within the ovaries. Furthermore, BBC3 was found to be not required for the massive germ cell loss that occurs during germ cell nest breakdown. Our data indicate that BBC3 is a critical regulator of germ cell death that acts during the migratory phase of oogenesis or very soon after the arrival of germ cells in the gonad and that BBC3-mediated cell death limits the number of primordial follicles established in the initial ovarian reserve.

scholarly journals Chromosome pairing and germ cell loss in male and female mice carrying a reciprocal translocation

Reproduction ◽  
1988 ◽  
Vol 82 (1) ◽  
pp. 369-379 ◽  
Author(s):  
L. A. Setterfield ◽  
S. Mahadevaiah ◽  
U. Mittwoch
Keyword(s):  
Germ Cell ◽  
Chromosome Pairing ◽  
Reciprocal Translocation ◽  
Cell Loss ◽  
Male And Female ◽  
Female Mice

001 Exploring the Orexin-tTA/TetO-DTA Mouse as a Model for Pediatric Narcolepsy

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A1-A1
Author(s):  
Adam Joyal ◽  
Akihiro Yamanaka ◽  
Thomas Scammell ◽  
Alissa Coffey
Keyword(s):  
Rem Sleep ◽  
Pediatric Population ◽  
Cell Loss ◽  
Adult Onset ◽  
Young Onset ◽  
Female Mice ◽  
Orexin Neuron ◽  
Entire Experiment ◽  
Diphtheria Toxin A ◽  
Selective Death

Abstract Introduction Narcolepsy is a sleep disorder caused by selective death of the orexin neurons that often begins in childhood. Orexin neuron loss disinhibits REM sleep during the active period and produces cataplexy, an abnormal behavioral state between REM sleep and wakefulness. Cataplexy is often more severe when narcolepsy develops in children compared to adults, but the mechanisms underlying this difference remain unknown. Methods We used orexin-tTA/TetO-DTA mice to model narcolepsy at different ages. When doxycycline is removed from the diet, the orexin neurons of these mice express diphtheria toxin A and die within 2–3 weeks. We removed doxycycline at 4 weeks (young-onset) or 14 weeks (adult-onset) of age in male and female mice. We implanted EEG and EMG electrodes for sleep recordings one week later and then recorded EEG/EMG/video for 24h at 3 and 13 weeks after removal of doxycycline. Age-matched controls had access to doxycycline diet for the entire experiment. Results Three weeks after doxycycline removal, both young-onset and adult-onset mice developed cataplexy and the sleep-wake fragmentation characteristic of narcolepsy. Age of orexin cell loss did not significantly affect cataplexy severity, however, female mice had more cataplexy than male mice overall. Both young- and adult-onset mice showed a 99% loss of orexin neurons at 3 weeks. Conclusion Considered together, our results suggest that the orexin-tTA/TetO-DTA mouse model of narcolepsy does not capture the severe cataplexy that is often seen in the human pediatric population. Support (if any):

scholarly journals Estrogen Receptor β Controls Muscle Growth and Regeneration in Young Female Mice

2020 ◽  
Vol 15 (3) ◽  
pp. 577-586 ◽  
Author(s):  
Daiki Seko ◽  
Ryo Fujita ◽  
Yuriko Kitajima ◽  
Kodai Nakamura ◽  
Yuuki Imai ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Muscle Growth ◽  
Young Female ◽  
Estrogen Receptor Β ◽  
Female Mice

scholarly journals Drosophila CG2469 Encodes a Homolog of Human CTR9 and Is Essential for Development

2016 ◽  
Vol 6 (12) ◽  
pp. 3849-3857 ◽  
Author(s):  
Dhananjay Chaturvedi ◽  
Mayu Inaba ◽  
Shane Scoggin ◽  
Michael Buszczak
Keyword(s):  
Germ Cell ◽  
Sequence Similarity ◽  
Cell Loss ◽  
Germline Stem Cell ◽  
Cell Nuclei ◽  
Transcriptional Initiation ◽  
Histone Locus Bodies ◽  
Paf1 Complex ◽  
Histone Locus ◽  
Drosophila Cells

Abstract Conserved from yeast to humans, the Paf1 complex participates in a number of diverse processes including transcriptional initiation and polyadenylation. This complex typically includes five proteins: Paf1, Rtf1, Cdc73, Leo1, and Ctr9. Previous efforts identified clear Drosophila homologs of Paf1, Rtf1, and Cdc73 based on sequence similarity. Further work showed that these proteins help to regulate gene expression and are required for viability. To date, a Drosophila homolog of Ctr9 has remained uncharacterized. Here, we show that the gene CG2469 encodes a functional Drosophila Ctr9 homolog. Both human and Drosophila Ctr9 localize to the nuclei of Drosophila cells and appear enriched in histone locus bodies. RNAi knockdown of Drosophila Ctr9 results in a germline stem cell loss phenotype marked by defects in the morphology of germ cell nuclei. A molecular null mutation of Drosophila Ctr9 results in lethality and a human cDNA CTR9 transgene rescues this phenotype. Clonal analysis in the ovary using this null allele reveals that loss of Drosophila Ctr9 results in a reduction of global levels of histone H3 trimethylation of lysine 4 (H3K4me3), but does not compromise the maintenance of stem cells in ovaries. Given the differences between the null mutant and RNAi knockdown phenotypes, the germ cell defects caused by RNAi likely result from the combined loss of Drosophila Ctr9 and other unidentified genes. These data provide further evidence that the function of this Paf1 complex component is conserved across species.

scholarly journals Extension of longevity and reduction of inflammation is ovarian-dependent, but germ cell-independent in post-reproductive female mice

GeroScience ◽  
2018 ◽  
Vol 41 (1) ◽  
pp. 25-38 ◽  
Author(s):  
Tracy L. Habermehl ◽  
Kate C. Parkinson ◽  
Gene B. Hubbard ◽  
Yuji Ikeno ◽  
Jennifer I. Engelmeyer ◽  
...  
Keyword(s):  
Germ Cell ◽  
Female Mice ◽  
Reproductive Female

Abstract 3710: Estrogen Does not Account for Accelerated Atherosclerosis in LDLr−/− Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Victoria L King ◽  
Nicholas Hatch ◽  
Xuan Zhang ◽  
Lisa R Tannock
Keyword(s):  
Body Weight Gain ◽  
Atherosclerotic Lesion ◽  
Young Female ◽  
Lesion Formation ◽  
Accelerated Atherosclerosis ◽  
Female Mice ◽  
Ldl Particles ◽  
Gender Specific Differences ◽  
Event Rates ◽  
Atherosclerotic Lesion Formation

Clinical studies demonstrate less atherosclerosis in pre-menopausal women compared to age-matched men, but an equalization in atherosclerosis burden and cardiovascular event rates between genders following menopause. Conversely, using the LDLR−/− mouse model we and others have previously demonstrated that young female mice develop accelerated atherosclerosis compared to age matched males. Whether this difference is due to sex hormones or differences in metabolic factors is not clear. To determine if estrogen mediated the alterations in atherosclerosis in the female mice, female mice were ovariectomized (Ovx). Ovx mice had a marked reduction in uterus weight (Sham: 86 ± 1 vs Ovx: 26 ± 1mg, P < 0.001) and both Ovx females and males had greater body weight gain when fed a lard-enriched diet (10% kcal from fat, D12451 , Research Diets) for 17 weeks compared to sham females. Ovariectomy resulted in an increase in fasting glucose concentrations, which was comparable to males. Cholesterol and triglyceride concentrations were higher in both sham and Ovx females compared to males; primarily distributed in increased VLDL and LDL particles. Interestingly, ovariectomy had no significant effect on extent of atherosclerotic lesion formation in female mice and the extent of atherosclerotic lesion area in both female groups was significantly increased compared to male mice. These data suggest that gender specific differences in lipids and atherosclerotic lesion formation in female LDL-R deficient mice fed a diet enriched in lard are not mediated by estrogen.

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