Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24798344_1.fastq.gz | Fastqsanger.gz | |||
| SRR24798344_2.fastq.gz | Fastqsanger.gz | |||
| SRR24798345_1.fastq.gz | Fastqsanger.gz | |||
| SRR24798345_2.fastq.gz | Fastqsanger.gz | |||
| SRR24798346_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Error profile of the DNA storage channel
| PRJEB32885 | ENA
Project description:Combinatorial DNA storage
| PRJEB71104 | ENA
Project description:DNA replication is sensitive to damage in the template. To bypass lesions and complete replication, cells activate recombination-mediated (error-free) and translesion synthesis-mediated (error-prone) DNA damage tolerance pathways. Crucial for error-free DNA damage tolerance is template switching, which depends on the formation and resolution of damage-bypass intermediates consisting of sister chromatid junctions. Here we show that a chromatin architectural pathway involving the high mobility group box protein Hmo1 channels replication-associated lesions into the error-free DNA damage tolerance pathway mediated by Rad5 and PCNA polyubiquitylation, while preventing mutagenic bypass and toxic recombination. In the process of template switching, Hmo1 also promotes sister chromatid junction formation predominantly during replication. Its C-terminal tail, implicated in chromatin bending, facilitates the formation of catenations/hemicatenations and mediates the roles of Hmo1 in DNA damage tolerance pathway choice and sister chromatid junction formation. Together, the results suggest that replication-associated topological changes involving the molecular DNA bender, Hmo1, set the stage for dedicated repair reactions that limit errors during replication and impact on genome stability.
2014-01-28 | GSE46260 | GEO
Project description:An enduring issue in evolutionary and cancer biology is how replication infidelity influences genome composition and vice versa. Here we examine this issue by sequencing the genomes of diploid budding yeast strains that are either mismatch repair (MMR) proficient or deficient and encode wild type or mutator variants of the three major nuclear DNA replicases. Analysis of over 43,000 mutations that accumulated in the absence of selective pressure demonstrates that the nuclear DNA replication machinery generates less than one mismatch per genome and in combination with MMR, achieves a genome-wide per base error rate of 1.7 x 10-10. Absent both MMR and purifying selection, replication error patterns strongly depend on replication origin proximity, replication fork direction, and the local DNA sequence. Preferred sequences were observed for base substitutions and deletions. Error rates also vary with replication time, in linker versus nucleosome-bound DNA, in 5'- and 3'-untranslated regions, in coding regions and in intergenic DNA. This genome-wide view shows that replication fidelity is amazingly high but heterogeneous, in patterns that suggest the underlying mechanisms by which replication modulates genome stability and composition and vice versa. Six to ten isolates were sequenced for each combination of DNA polymerase (WT, pol1-L868M, pol2-M644G, pol3-L612M) and mismatch repair (proficient, deficient) genotypes. A single WT isolate was sequenced following micrococcal nuclease digestion.
2014-08-25 | E-GEOD-56939 | biostudies-arrayexpress
Project description:An enduring issue in evolutionary and cancer biology is how replication infidelity influences genome composition and vice versa. Here we examine this issue by sequencing the genomes of diploid budding yeast strains that are either mismatch repair (MMR) proficient or deficient and encode wild type or mutator variants of the three major nuclear DNA replicases. Analysis of over 43,000 mutations that accumulated in the absence of selective pressure demonstrates that the nuclear DNA replication machinery generates less than one mismatch per genome and in combination with MMR, achieves a genome-wide per base error rate of 1.7 x 10-10. Absent both MMR and purifying selection, replication error patterns strongly depend on replication origin proximity, replication fork direction, and the local DNA sequence. Preferred sequences were observed for base substitutions and deletions. Error rates also vary with replication time, in linker versus nucleosome-bound DNA, in 5'- and 3'-untranslated regions, in coding regions and in intergenic DNA. This genome-wide view shows that replication fidelity is amazingly high but heterogeneous, in patterns that suggest the underlying mechanisms by which replication modulates genome stability and composition and vice versa.
2014-08-25 | GSE56939 | GEO
Project description:This is a biological replicate of EV59+60. The purpose of the chromatin immunoprecipitation/microarray (ChIP/chip) experiment is to determine which regions of a genome are enriched for a particular histone modification in a single Arabidopsis thanliana genotype. Chromatin immunoprecipitation with antibodies raised against dimethyl histone-H3 lysine-9 (H3mK9) or dimethyl histone-H3 lysine-4 (H3mK4) is performed on a selected genotype. This purified DNA from each immunoprecipiation (mH3K9, mH3K4, no antibody control) is used for random amplification to increase the quantity of DNA for microarray hybridization. The amplified DNA from each experimental sample is then labeled with Cy5 and hybridized against total input DNA from the corresponding genotype, labeled in Cy3. In a single hybridization, the total input DNA serves as a baseline and is compared to the immunoprecipitated samples. Ratios of normalized signal intensities were calculated to identify enrichment of a particular sequence after immunoprecipitation, in comparison to the total input DNA. Dye swap analysis is carried out to take account of experimental variation by repeating the hybridization with identical samples labeled with Cy3 and Cy5, respectively. The two samples in this series are complementary hybridizations in a dye-swap analysis. These data were normalized and subjected to hypothesis testing. Error rate was controlled by Benjamini and Hochberg's step-up procedure for limiting the False Discovery Rate. Wild-type seedlings, 9 days old This is the normalized result of the paired dye swap samples EV110 and EV111. The ANOVA model of Kerr, Martin and Churchill (2000) was used to analyze the data from the dye-swap experiments, with terms included to account for gene, dye-by-gene, treatment-by-gene, and random error terms. The style of hypothesis test proposed by Black and Doerge (2002) was applied to each of the features represented on each array, with rejection of the null hypothesis indicating a significant change in fluorescence intensity. To account for the number of hypothesis tests being made, and thus provide some level of error rate control, significance was assessed using false discovery rate (FDR) controlling methods. The step-up procedure of Benjamini and Hochberg (1995) was used to control the FDR below alpha = 0.01. For the purposes of this experiment, the hypotheses were assumed to be independent. Features found after hypothesis-testing with a controlled error rate to be significantly enriched or depleted for H3K9 methylation compared to mean values found in euchromatic regions are flagged in the column. No family-wise error rate methods were used to analyze this sample. Keywords: other
2004-06-12 | GSE1340 | GEO