scholarly journals The EEL-1 ubiquitin ligase promotes DNA damage-induced germ cell apoptosis in C. elegans

2011 ◽  
Vol 18 (7) ◽  
pp. 1140-1149 ◽  
Author(s):  
A J Ross ◽  
M Li ◽  
B Yu ◽  
M X Gao ◽  
W B Derry
Keyword(s):  
Dna Damage ◽  
Germ Cell ◽  
Ubiquitin Ligase ◽  
Cell Apoptosis ◽  
Germ Cell Apoptosis ◽  
C Elegans

scholarly journals Autophagy of germ-granule components, PGL-1 and PGL-3, contributes to DNA damage-induced germ cell apoptosis in C. elegans

PLoS Genetics ◽  
2019 ◽  
Vol 15 (5) ◽  
pp. e1008150 ◽  
Author(s):  
Hyemin Min ◽  
Yong-Uk Lee ◽  
Yhong-Hee Shim ◽  
Ichiro Kawasaki
Keyword(s):  
Dna Damage ◽  
Germ Cell ◽  
Cell Apoptosis ◽  
Germ Cell Apoptosis ◽  
C Elegans

scholarly journals 4-Bromodiphenyl Ether Induces Germ Cell Apoptosis by Induction of ROS and DNA Damage in Caenorhabditis elegans

2017 ◽  
Vol 157 (2) ◽  
pp. 510-518 ◽  
Author(s):  
Xinyue You ◽  
Jing Xi ◽  
Yiyi Cao ◽  
Jinfu Zhang ◽  
Yang Luan
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Cell Apoptosis ◽  
Germ Cell Apoptosis

scholarly journals Isoflurane impairs oogenesis through germ cell apoptosis in C. elegans

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tao Zhang ◽  
Cheng Ni ◽  
Cheng Li ◽  
Pan Lu ◽  
Dan Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Germ Cell ◽  
Fluorescence Imaging ◽  
Cell Apoptosis ◽  
Germ Cell Apoptosis ◽  
C Elegans ◽  
Interaction Studies ◽  
Acetyl Cysteine ◽  
Induced Changes ◽  
And Oxidative Stress

AbstractAnesthetic isoflurane has been reported to induce toxicity. However, the effects of isoflurane on fecundity remain largely unknown. We established a system in C. elegans to investigate the effects of isoflurane on oogenesis. Synchronized L4 stage C. elegans were treated with 7% isoflurane for 4 h. Dead cells, ROS, embryos, and unfertilized eggs laid by hermaphrodites were measured by fluorescence imaging and counting. The C. elegans with losses of ced-3, cep-1, abl-1, male C. elegans, and oxidative stress inhibitor N-acetyl-cysteine were used in the interaction studies. We found that isoflurane decreased the numbers of embryos and unfertilized eggs and increased the levels of dead cells and ROS in C. elegans. The isoflurane-induced impairment of oogenesis was associated with abl-1, ced-3, but not cep-1. N-acetyl-cysteine attenuated the isoflurane-induced impairment of oogenesis in C. elegans. Mating with male C. elegans did not attenuate the isoflurane-induced changes in oogenesis. These findings suggest that isoflurane may impair oogenesis through abl-1- and ced-3-associated, but not cep-1-associated, germ cell apoptosis and oxidative stress, pending further investigation. These studies will promote more research to determine the potential effects of anesthesia on fecundity.

scholarly journals Mutation of a Nopp140 gene dao-5 alters rDNA transcription and increases germ cell apoptosis in C. elegans

2014 ◽  
Vol 5 (4) ◽  
pp. e1158-e1158 ◽  
Author(s):  
C-C Lee ◽  
Y-T Tsai ◽  
C-W Kao ◽  
L-W Lee ◽  
H-J Lai ◽  
...  
Keyword(s):  
Germ Cell ◽  
Cell Apoptosis ◽  
Rdna Transcription ◽  
Germ Cell Apoptosis ◽  
C Elegans

scholarly journals Genome-wide RNAi identifies p53-dependent and -independent regulators of germ cell apoptosis in C. elegans

2004 ◽  
Vol 11 (11) ◽  
pp. 1198-1203 ◽  
Author(s):  
G Lettre ◽  
E A Kritikou ◽  
M Jaeggi ◽  
A Calixto ◽  
A G Fraser ◽  
...  
Keyword(s):  
Germ Cell ◽  
Cell Apoptosis ◽  
Germ Cell Apoptosis ◽  
C Elegans ◽  
Genome Wide

scholarly journals JNK inhibition alleviates oxidative DNA damage, germ cell apoptosis, and mitochondrial dysfunction in testicular ischemia reperfusion injury

2020 ◽  
Vol 52 (8) ◽  
pp. 891-900
Author(s):  
Fatemah Fadel ◽  
Nora Al-Kandari ◽  
Farah Khashab ◽  
Farah Al-Saleh ◽  
May Al-Maghrebi
Keyword(s):  
Dna Damage ◽  
Germ Cell ◽  
Mitochondrial Dysfunction ◽  
Cell Apoptosis ◽  
Oxidative Dna Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Jnk Signaling ◽  
Germ Cell Apoptosis ◽  
Testicular Ischemia

Abstract The aim of this study is to determine whether the c-Jun N-terminal kinase (JNK) signaling is a regulator of oxidative DNA damage, germ cell apoptosis (GCA), and mitochondrial dysfunction during testicular ischemia reperfusion injury (tIRI) using the JNK inhibitor SP600125. Male Sprague Dawley rats (n = 36) were equally divided into three groups: sham, tIRI only, and tIRI + SP600125 (15 mg/kg). Testicular ischemia was induced for 1 h followed by 4 h of reperfusion prior to animal sacrifice. Spermatogenesis was evaluated by light microscopy, while expression of oxidative stress and GCA-related mRNAs and proteins were evaluated by real-time polymerase chain reaction and colorimetric assays, respectively. Expressions of JNK, p53, and survivin were detected by immunofluorescence (IF) staining. Indicators of mitochondrial dysfunction were examined by western blot analysis and colorimetric assay. In comparison to sham, the tIRI testes showed a significant increase in lipid and protein oxidation products. Oxidative DNA damage was reflected by a significant increase in the number of DNA strand breaks, increased concentration of 8-OHdG, and elevated poly (ADP-ribose) polymerase activity. Spermatogenic damage was associated with the activation of caspase 3 and elevated Bax to Bcl2 ratio. This was also accompanied by a significantly heightened IF expression of the phosphorylated forms of JNK and p53 paralled with the suppression of survivin. Mitochondrial dysfunction was reflected by NAD+ depletion, overexpression of uncoupling protein 2, and increased level of cytochrome c. Such tIRI-induced modulations were all attenuated by SP600125 treatment prior to reperfusion. In conclusion, JNK signaling regulates oxidative DNA damage, GCA, and mitochondrial dysfunction through activation of p53 and suppression of survivin during tIRI.

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