RNaseH2A Downregulation Drives Chromosomal DNA Fragmentation and Accumulation of RNA-DNA Hybrids in Senescent Cells

2020 ◽  
Author(s):  
Ryo Okada ◽  
Sho Sugawara ◽  
Tze Mun Loo ◽  
Kenichi Miyata ◽  
Kaoru Kato ◽  
...  
Keyword(s):  
Dna Fragmentation ◽  
Chromosomal Dna

Endonuclease Activation and Chromosomal DNA Fragmentation during Apoptosis in Leukemia Cells

2006 ◽  
Vol 84 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Akira Yoshida ◽  
Yves Pommier ◽  
Takanori Ueda
Keyword(s):  
Dna Fragmentation ◽  
Leukemia Cells ◽  
Chromosomal Dna

Assessment of Chromosomal DNA Fragmentation by Quinolones in an Isogenic Collection of Escherichia coli with Defined Resistance Mechanisms

2016 ◽  
Vol 22 (5) ◽  
pp. 354-359 ◽  
Author(s):  
José-Manuel Rodríguez-Martínez ◽  
Rebeca Santiso ◽  
Jesús Machuca ◽  
Germán Bou ◽  
Álvaro Pascual ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Fragmentation ◽  
Resistance Mechanisms ◽  
Chromosomal Dna

Cell wall active antibiotics reduce chromosomal DNA fragmentation by peptidoglycan hydrolysis in Staphylococcus aureus

2012 ◽  
Vol 194 (12) ◽  
pp. 967-975 ◽  
Author(s):  
María Tamayo ◽  
Rebeca Santiso ◽  
Jaime Gosálvez ◽  
Germán Bou ◽  
María del Cármen Fernández ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Dna Fragmentation ◽  
Chromosomal Dna ◽  
Peptidoglycan Hydrolysis

scholarly journals In VitroUltrastructural Changes of MCF-7 for Metastasise Bone Cancer and Induction of Apoptosis via Mitochondrial Cytochrome C Released by CaCO3/Dox Nanocrystals

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Abdullahi Shafiu Kamba ◽  
Maznah Ismail ◽  
Tengku Azmi Tengku Ibrahim ◽  
Zuki Abu Bakar Zakaria ◽  
Lawal Hassan Gusau
Keyword(s):  
Breast Cancer ◽  
Cytochrome C ◽  
Dna Fragmentation ◽  
Morphological Changes ◽  
Chromatin Condensation ◽  
Bone Cancer ◽  
Breast Cancers ◽  
Chromosomal Dna ◽  
Substantial Impact ◽  
Mcf 7

Bones are the most frequent site for breast cancer cells to settle and spread (metastasise); bone metastasis is considered to have a substantial impact on the quality of patients with common cancers. However, majority of breast cancers develop insensitivity to conventional chemotherapy which provides only palliation and can induce systemic side effects. In this study we evaluated the effect of free Dox and CaCO3/Dox nanocrystal on MCF-7 breast cancer using MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide), neural red, and lactate dehydrogenase colorimetric assays while DNA fragmentation and BrdU genotoxicity were also examined. Apoptogenic protein Bax, cytochrome C, and caspase-3 protein were analysed. Morphological changes of MCF-7 were determined using contrast light microscope and scanning and transmission electron microscope (SEM and TEM). The findings of the analysis revealed higher toxicity of CaCO3/Dox nanocrystal and effective cells killing compared to free Dox, morphological changes such as formation of apoptotic bodies, membrane blebbing, and absent of microvilli as indicated by the SEM analysis while TEM revealed the presence of chromatin condensation, chromosomal DNA fragmentation, cell shrinkage, and nuclear fragmentation. Results of TUNEL assay verified that most of the cells undergoes apoptosis by internucleosomal fragmentation of genomic DNA whereas the extent of apoptotic cells was calculated using the apoptotic index (AI). Therefore, the biobased calcium carbonate nanocrystals such as Dox carriers may serve as an alternative to conventional delivery system.

scholarly journals Molecular cloning and characterization of human caspase-activated DNase

1998 ◽  
Vol 95 (16) ◽  
pp. 9123-9128 ◽  
Author(s):  
Naomi Mukae ◽  
Masato Enari ◽  
Hideki Sakahira ◽  
Yoji Fukuda ◽  
Johji Inazawa ◽  
...  
Keyword(s):  
Dna Fragmentation ◽  
Cell Lines ◽  
Point Mutations ◽  
Leukemic Cell ◽  
Coding Region ◽  
Chromosomal Dna ◽  
Caspase Activated Dnase

Caspase-activated DNase (CAD) cleaves chromosomal DNA during apoptosis. Here, we report isolation of two classes of human CAD cDNAs from a human KT-3 leukemic cell cDNA library. One class of cDNA encoded a protein comprising 338 amino acids, which showed a marked similarity to its murine counterpart. In vitro transcription and translation of this cDNA resulted in a functional CAD protein when the protein was synthesized in the presence of its inhibitor (inhibitor of CAD). The other cDNA class contained many deletions, insertions, and point mutations in the sequence corresponding to the coding region, suggesting that it is derived from a pseudogene. The functional CAD gene was localized to human chromosome 1p36.3 by fluorescent in situ hybridization. The CAD mRNA was expressed in a limited number of human tissues, including pancreas, spleen, prostate, and ovary. The expression of the CAD mRNA in human cell lines correlated with their ability to show DNA fragmentation during apoptosis. Overexpression of CAD potentiated DNA fragmentation by apoptotic stimuli in these cell lines, indicating that CAD is responsible for the apoptotic DNA degradation.

scholarly journals An auxiliary mode of apoptotic DNA fragmentation provided by phagocytes

2000 ◽  
Vol 14 (5) ◽  
pp. 549-558 ◽  
Author(s):  
Dorian McIlroy ◽  
Masato Tanaka ◽  
Hideki Sakahira ◽  
Hidehiro Fukuyama ◽  
Misao Suzuki ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Dna Fragmentation ◽  
Apoptotic Cells ◽  
Wild Type ◽  
Chromosomal Dna ◽  
Γ Irradiation ◽  
Dnase Ii ◽  
Striking Increase ◽  
Resistant Form ◽  
Acid Dnase

CAD (caspase-activated DNase) can cause DNA fragmentation in apoptotic cells. Transgenic mice that ubiquitously express a caspase-resistant form of the CAD inhibitor (ICAD) were generated. Thymocytes prepared from the mice were resistant to DNA fragmentation induced by a variety of stimuli. However, similar numbers of TUNEL-positive cells were present in adult tissues of transgenic and wild-type mice. Exposure to γ-irradiation caused a striking increase in the number of TUNEL-positive cells in the thymus of wild-type, but not transgenic, mice. TUNEL-positive nuclei in transgenic mice were confined to thymic macrophages. When apoptotic thymocytes from the transgenic mice were cocultured with macrophages, the thymocytes underwent phagocytosis and their chromosomal DNA underwent fragmentation. This DNA fragmentation was sensitive to inhibitors that block the acidification of lysosomes. Hence, we conclude that the DNA fragmentation that occurs during apoptosis not only can result cell-autonomously from CAD activity but can also be attributed to a lysosomal acid DNase(s), most likely DNase II, after the apoptotic cells are engulfed.

scholarly journals Characterization of DNA Damage in Yeast Apoptosis Induced by Hydrogen Peroxide, Acetic Acid, and Hyperosmotic Shock

2006 ◽  
Vol 17 (10) ◽  
pp. 4584-4591 ◽  
Author(s):  
Gabriela F. Ribeiro ◽  
Manuela Côrte-Real ◽  
Björn Johansson
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Acetic Acid ◽  
Dna Fragmentation ◽  
Tunel Staining ◽  
Chromosomal Dna ◽  
Dna Breaks ◽  
Hyperosmotic Shock ◽  
Double Strand Dna Breaks

Saccharomyces cerevisiae has been reported to die, under certain conditions, from programmed cell death with apoptotic markers. One of the most important markers is chromosomal DNA fragmentation as indicated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. We found TUNEL staining in S. cerevisiae to be a consequence of both single- and double-strand DNA breaks, whereas in situ ligation specifically stained double-strand DNA breaks. Cells treated with hydrogen peroxide or acetic acid staining positively for TUNEL assay stained negatively for in situ ligation, indicating that DNA damage in both cases mainly consists of single-strand DNA breaks. Pulsed field gel electrophoresis of chromosomal DNA from cells dying from hydrogen peroxide, acetic acid, or hyperosmotic shock revealed DNA breakdown into fragments of several hundred kilobases, consistent with the higher order chromatin degradation preceding DNA laddering in apoptotic mammalian cells. DNA fragmentation was associated with death by treatment with 10 mM hydrogen peroxide but not 150 mM and was absent if cells were fixed with formaldehyde to eliminate enzyme activity before hydrogen peroxide treatment. These observations are consistent with a process that, like mammalian apoptosis, is enzyme dependent, degrades chromosomal DNA, and is activated only at low intensity of death stimuli.

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