1,720,998 research outputs found
The organization of classical satellite DNAs in human chromosomes: an approach using Ulul and Taql restriction endonucleases
No full textSome remarks on the use of TaqI to detect highly repetitive DNA sequences in human chromosomes
No full textIn the attempt to conclude investigation of the action of restriction endonucleases on eukaryote chromosomes, we carried out a series of experiments digesting in situ human metaphase chromosomes with AluI/TaqI followed by Giemsa staining. We focused on the centromeric regions of chromosomes1, 2 and 16 and noted that those areas appeared as intensely stained blocks after AluI digestion, but were dramatically reduced in size or completely destroyed after subsequent TaqI treatment. These results permitted us to draw some conclusions on the highly repetitive DNA composition of these regions, in terms of alphoid and classical satellite DNAs
The impact of StuI digestion in situ on FISH to human chromosomes with satellite DNA probes
No full textHuman metaphase chromosomes were digested with Stul and subsequently hybridized in situ using chromosome 9 alphoid DNA and classical satellite III DNA as probes. The data obtained suggest that it is not possible to establish a general rule regarding the cytological effects induced by restriction enzymes in particular chromosome regions and that a number of factors, such as DNA sequences, DNA-protein interaction and enzyme structure, play a role in determining such effects
On the variability of MboI repeated sequences and 5S rDNA in Muraena helena and Gymnothorax unicolor ( Anguilliformes, Muraenide )
No full textOn the variability of MboI repeated sequences and 5S rDNA in Muraena helena and Gymnotorax unicolor (Anguilliformes, Muraenidae)
No full textKaryotype characterization and comparison in moray eels (Anguilliformes, Muraenidae).
No full textThe karyotype of the teleostean Gymnothorax tile was analysed by replication banding in order to clearly identify the homologous chromosomes. The RBG pattern was then compared to those of the other Muraenidae studied (G. unicolor and Muraena helena) and banding homologies of nine chromosome pairs were pointed out. A single nucleolar organizer region (NOR) was localized by FISH, silver- and CMA3-staining on the short arm of the pair 12. Telomeric (TTAGGG) repeats were terminally localized by FISH on all the chromosome pairs. The genome size and the AT-DNA content were evaluated by flow cytometry. Available cytogenetic data on the Muraenidae were then compared and discussed
The efficiency of in-situ hybridization on human chromosomes with alphoid DNAs is enhanced by previous digestion with AluI and TaqI
No full textMitochondria morphology and DNA content upon sublethal exposure to beta-amyloid(1-42) peptide
No full textBrains affected by Alzheimer's disease (AD) show a large spectrum of mitochondrial alterations at both morphological and genetic level. The causal link between amyloid beta peptides (AP) and mitochondrial dysfunction has been established in cellular models of AD using Abeta concentrations capable of triggering massive neuronal death. However, mitochondrial changes related to sublethal exposure to Abeta are less known. Here we show that subtoxic, 1 microM Abeta(1-42) exposure does not change the mitochondrial shape of living cells, as visualized upon the uptake of the non-potentiometric fluorescent probe Mitotracker Green and enhanced yellow fluorescent protein (EYFP)-tagged cytochrome c oxidase expression. Immunolocalization of oxidative adducts 8-hydroxy-2'-deoxyguanosine, 8-hydroxyguanine and 8-hydroxyguanosine demonstrates that one-micromolar concentration of Abeta(1-42) is also not sufficient to elicit dramatic qualitative changes in the RNA/DNA oxidative products. However, in comparison with controls, semi-quantitative analysis of the overall mitochondrial mass by integrated fluorescence intensity reveals an ongoing down-regulation in mitochondrial biosynthesis or, conversely, an enhanced autophagic demise of Abeta treated cells. Furthermore, a significant increase of the full-length mitochondrial DNA (mtDNA) from Abeta-treated versus control cells is found, as measured by long range polymerase chain reaction (PCR). Such up-regulation is accompanied by extensive fragmentation of the unamplified mtDNA, probably due to the detrimental effect of Abeta. We interpret these results as a sequence of compensatory responses induced by mtDNA damage, which are devoted to repression of oxidative burst. In conclusion, our findings suggest that early therapeutic interventions aimed at prevention of mitochondrial oxidative damage may delay AD progression and help in treating AD patients
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