DNA migration through semi-circular gradient channel

2021 ◽  
pp. 126573
Author(s):  
Dibyajyoti Mohanta
Keyword(s):  
Dna Migration ◽  
Gradient Channel

scholarly journals Maintenance of Mitochondrial Morphology Is Linked to Maintenance of the Mitochondrial Genome in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 162 (3) ◽  
pp. 1147-1156 ◽  
Author(s):  
Theodor Hanekamp ◽  
Mary K Thorsness ◽  
Indrani Rebbapragada ◽  
Elizabeth M Fisher ◽  
Corrine Seebart ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Growth Rate ◽  
Mitochondrial Dna ◽  
Carbon Sources ◽  
Mitochondrial Morphology ◽  
Yeast Saccharomyces Cerevisiae ◽  
Slow Growth Rate ◽  
Dna Migration ◽  
Mitochondrial Dna Stability ◽  
Extragenic Suppressors

Abstract In the yeast Saccharomyces cerevisiae, certain mutant alleles of YME4, YME6, and MDM10 cause an increased rate of mitochondrial DNA migration to the nucleus, carbon-source-dependent alterations in mitochondrial morphology, and increased rates of mitochondrial DNA loss. While single mutants grow on media requiring mitochondrial respiration, any pairwise combination of these mutations causes a respiratory-deficient phenotype. This double-mutant phenotype allowed cloning of YME6, which is identical to MMM1 and encodes an outer mitochondrial membrane protein essential for maintaining normal mitochondrial morphology. Yeast strains bearing null mutations of MMM1 have altered mitochondrial morphology and a slow growth rate on all carbon sources and quantitatively lack mitochondrial DNA. Extragenic suppressors of MMM1 deletion mutants partially restore mitochondrial morphology to the wild-type state and have a corresponding increase in growth rate and mitochondrial DNA stability. A dominant suppressor also suppresses the phenotypes caused by a point mutation in MMM1, as well as by specific mutations in YME4 and MDM10.

Chlorinated river and lake water extract caused oxidative damage, DNA migration and cytotoxicity in human cells

2005 ◽  
Vol 208 (6) ◽  
pp. 481-488 ◽  
Author(s):  
Jing Yuan ◽  
Xin-Jiang Wu ◽  
Wen-Qing Lu ◽  
Xiao-Li Cheng ◽  
Dan Chen ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Lake Water ◽  
Water Extract ◽  
Human Cells ◽  
Dna Migration

Is the natural PCDD/PCDF mixture toxic for human placental JEG-3 cell line? The action of the toxicants on hormonal profile, CYP1A1 activity, DNA damage and cell apoptosis

2007 ◽  
Vol 26 (5) ◽  
pp. 407-417 ◽  
Author(s):  
Katarzyna Augustowska ◽  
Zofia Magnowska ◽  
Maria Kapiszewska ◽  
Ewa L. Gregoraszczuk
Keyword(s):  
Dna Damage ◽  
Cell Line ◽  
Cell Apoptosis ◽  
Hormone Production ◽  
Dna Migration ◽  
Extraction And Purification ◽  
Cyp1a1 Expression ◽  
Cross Links ◽  
Placental Hormone

The present study was conducted to define the action of a mixture obtained by the extraction and purification of real fly ash, on specific toxicity endpoints, such as hormonal secretion, CYP1A1 expression, DNA damage and cell apoptosis. JEG-3 cell line was exposed in vitro to different doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or Polychlorinated dibenzo-p-dioxin/Polychlorinated dibenzo-P-furan (PCDD/PCDF) mixture. Both TCDD and the mixture decreased hCG secretion, while inhibition of progesterone levels was noted only under the influence of TCDD. The changes in hormone production were not due to the action on cell viability. There were time-dependent differences in CYP1A1 expression in cells exposed to TCDD and PCDD/PCDF mixture. Both TCDD and PCDD/PCDF mixture did not induce the DNA damage, as evaluated by the comet assay. Significantly lower DNA migration from the head of comet into the comet tail was noted after the removal of reagents. The highest efficiency of this process was noted 4 h after the TCDD and 24 h after the PCDD/PCDF mixture removal. These results suggest that the DNA adducts and/or DNA—DNA cross-links were formed. Neither TCDD nor PCDD/PCDF mixture had any effect on cell apoptosis assessed by caspase-3 activity and Hoechst 33258. Taken together, these findings clearly indicate a weaker action of the mixture when compared with TCDD. However, in both cases, their action was not due to the induction of the DNA damage and subsequent cell apoptosis but due to a direct influence of these toxicants on placental hormone production. Human & Experimental Toxicology ( 2007) 26, 407—417

Dynamics of single-stranded DNA migration in denaturing polyacrylamide slab-gel electrophoresis

2001 ◽  
Vol 22 (16) ◽  
pp. 3527-3532 ◽  
Author(s):  
Zahia Djouadi ◽  
Samuele Bottani ◽  
Marie-Alix Duval ◽  
Rainer Siebert ◽  
Hrvé Tricoire ◽  
...  
Keyword(s):  
Gel Electrophoresis ◽  
Single Stranded Dna ◽  
Dna Migration

Impacts of small woody debris on slurrying, persistence, and propagation in a low-gradient channel of the Dongyuege debris flow in Nu River, Southwest China

Landslides ◽  
2018 ◽  
Vol 15 (11) ◽  
pp. 2279-2293 ◽  
Author(s):  
Yong-Jun Tang ◽  
Ze-Min Xu ◽  
Tai-Qiang Yang ◽  
Zhen-Hua Zhou ◽  
Kun Wang ◽  
...  
Keyword(s):  
Debris Flow ◽  
Southwest China ◽  
Woody Debris ◽  
Gradient Channel ◽  
Nu River ◽  
Small Woody Debris

DNA damage induced by phenylalanine and its analogue p-chlorophenylalanine in blood and brain of rats subjected to a model of hyperphenylalaninemia

2013 ◽  
Vol 91 (5) ◽  
pp. 319-324 ◽  
Author(s):  
Kellen R. Simon ◽  
Rosane M. dos Santos ◽  
Giselli Scaini ◽  
Daniela D. Leffa ◽  
Adriani P. Damiani ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cerebral Cortex ◽  
Phenylalanine Hydroxylase ◽  
Neurological Dysfunction ◽  
Control Group ◽  
Acute Administration ◽  
Dna Migration ◽  
In Vitro Effects

Phenylketonuria (PKU) is a disease caused by a deficiency of phenylalanine hydroxylase (PAH), resulting in an accumulation of phenylalanine (Phe) in the brain tissue, cerebrospinal fluid, and other tissues of PKU patients. Considering that high levels of Phe are associated with neurological dysfunction and that the mechanisms underlying the neurotoxicity in PKU remain poorly understood, the main objective of this study was to investigate the in vivo and in vitro effects of Phe on DNA damage, as determined by the alkaline comet assay. The results showed that, compared to control group, the levels of DNA migration were significantly greater after acute administration of Phe, p-chlorophenylalanine (p-Cl-Phe, an inhibitor of PAH), or a combination thereof in cerebral cortex and blood, indicating DNA damage. These treatments also provoked increase of carbonyl content. Additionally, when Phe or p-Cl-Phe was present in the incubation medium, we observed an increase in the frequency and index of DNA damage in the cerebral cortex and blood, without affecting lactate dehydrogenase (LDH) release. Our in vitro and in vivo findings indicate that DNA damage occurs in the cerebral cortex and blood of rats receiving Phe, suggesting that this mechanism could be, at least in part, responsible for the neurological dysfunction in PKU patients.

scholarly journals Is the Comet Assay a Sensitive Procedure for Detecting Genotoxicity?

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Satomi Kawaguchi ◽  
Takanori Nakamura ◽  
Ayumi Yamamoto ◽  
Gisho Honda ◽  
Yu F. Sasaki
Keyword(s):  
Comet Assay ◽  
Mammalian Cells ◽  
Positive Response ◽  
Micronucleus Test ◽  
Strand Breaks ◽  
Low Level ◽  
Genotoxic Potential ◽  
Dna Migration ◽  
Single Strand Breaks ◽  
Methyl Nitrosourea

Although the Comet assay, a procedure for quantitating DNA damage in mammalian cells, is considered sensitive, it has never been ascertained that its sensitivity is higher than the sensitivity of other genotoxicity assays in mammalian cells. To determine whether the power of the Comet assay to detect a low level of genotoxic potential is superior to those of other genotoxicity assays in mammalian cells, we compared the results of Comet assay with those of micronucleus test (MN test). WTK1 human lymphoblastoid cells were exposed to methyl nitrosourea (MNU), ethyl nitrosourea (ENU), methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS), bleomycin (BLM), or UVC. In Comet assay, cells were exposed to each mutagen with (Comet assay/araC) and without (Comet assay) DNA repair inhibitors (araC and hydroxyurea). Furthermore, acellular Comet assay (acellular assay) was performed to determine how single-strand breaks (SSBs) as the initial damage contributes to DNA migration and/or to micronucleus formation. The lowest genotoxic dose (LGD), which is defined as the lowest dose at which each mutagen causes a positive response on each genotoxicity assay, was used to compare the power of the Comet assay to detect a low level of genotoxic potential and that of MN test; that is, a low LGD indicates a high power. Results are summarized as follows: (1) for all mutagens studied, LGDs were MN test ≦ Comet assay; (2) except for BLM, LGDs were Comet assay/araC ≦ MN test; (3) except for UVC and MNU, LGDs were acellular assay ≦ Comet assay/araC ≦ MN test ≦ Comet assay. The following is suggested by the present findings: (1) LGD in the Comet assay is higher than that in MN test, which suggests that the power of the MN test to detect a low level of genotoxic potential is superior to that of the Comet assay; (2) for the studied mutagens, all assays were able to detect all mutagens correctly, which suggests that the sensitivity of the Comet assay and that of the MN test were exactly identical; (3) the power of the Comet assay to detect a low level of genotoxic potential can be elevated to a level higher than that of MN test by using DNA resynthesis inhibitors, such as araC and HU.

Sign in / Sign up

Export Citation Format

Share Document