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234 results for “double stranded breaks”
Data sets for modeling double strand break susceptibility and interrogating structural variation in cancer
<p>This is data used and produced for the study of "Modeling double strand break susceptibility to interrogate structural variation in cancer". </p> <p><strong>Background: </strong>Structural variants (SVs) are known to play important roles in a variety of cancers, but their origins and functional consequences are still poorly understood. Many SVs are thought to emerge from errors in the repair processes following DNA double strand breaks (DSBs).</p> <p><strong>Results:</strong> We used experimentally quantified DSB frequencies in cell lines with matched chromatin and sequence features to derive the first quantitative genome-wide models of DSB susceptibility. These models are accurate and provide novel insights into the mutational mechanisms generating DSBs. Models trained in one cell type can be successfully applied to others, but a substantial proportion of DSBs appear to reflect cell type specific processes. Using model predictions as a proxy for susceptibility to DSBs in tumours, many SV-enriched regions appear to be poorly explained by selectively neutral mutational bias alone. A substantial number of these regions show unexpectedly high SV breakpoint frequencies given their predicted susceptibility to mutation and are therefore credible targets of positive selection in tumours. These putatively positively selected SV hotspots are enriched for genes previously shown to be oncogenic. In contrast, several hundred regions across the genome show unexpectedly low levels of SVs, given their relatively high susceptibility to mutation. These novel coldspot regions appear to be subject to purifying selection in tumours and are enriched for active promoters and enhancers.</p> <p><strong>Conclusions:</strong> We conclude that models of DSB susceptibility offer a rigorous approach to the inference of SVs putatively subject to selection in tumours.</p>
Raw data of "Bridging of nucleosome-proximal DNA double-strand breaks by PARP2 enhances its interaction with HPF1"
<p>Raw data used in the following article:</p> <p>Bridging of nucleosome-proximal DNA double-strand breaks by PARP2 enhances its interaction with HPF1</p> <p>Guillaume Gaullier, Genevieve Roberts, Uma M. Muthurajan, Samuel Bowerman, Johannes Rudolph, Jyothi Mahadevan, Asmita Jha, Purushka S. Rae, Karolin Luger</p> <p>bioRxiv 846618; doi: <a href="https://doi.org/10.1101/846618">https://doi.org/10.1101/846618</a></p> <p>This includes:</p> <ul> <li>uncropped and unaltered images of all SDS-PAGE and native PAGE</li> <li>all size exclusion chromatograms and light scattering data</li> <li>raw data of all fluorescence polarization and FRET binding curves</li> <li>thermal shif assay raw data</li> </ul>
Data from: Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
Open the record for dataset details and reuse information.
Microscopy data from: Identification of genetic interactions with priB links the PriA/PriB DNA replication restart pathway to double-strand DNA break repair in Escherichia coli
<p>Collisions between DNA replication complexes (replisomes) and impediments such as damaged DNA or proteins tightly bound to the chromosome lead to premature dissociation of replisomes at least once per cell cycle in <em>Escherichia coli</em>. Left unrepaired, these events produce incompletely replicated chromosomes that cannot be properly partitioned into daughter cells. DNA replication restart, the process that reloads replisomes at prematurely terminated sites, is therefore essential in <em>E. coli</em> and other bacteria. Three replication restart pathways have been identified in <em>E. coli</em>: PriA/PriB, PriA/PriC, and PriC/Rep. A limited number of genetic interactions between replication restart and other genome maintenance pathways have been defined, but a systematic study placing replication restart reactions in a broader cellular context has not been performed. We have utilized transposon insertion sequencing to identify new genetic interactions between DNA replication restart pathways and other cellular systems. Known genetic interactors with the <em>priB</em> replication restart gene (uniquely involved in the PriA/PriB pathway) were confirmed and several novel <em>priB </em>interactions were discovered. Far fewer connections were found with the PriA/PriC or PriC/Rep pathways, suggesting a primacy role for the PriA/PriB pathway in <em>E. coli</em>. Targeted genetic and imaging-based experiments with <em>priB</em> and its genetic partners revealed significant double-strand DNA break (DSB) accumulation in strains with mutations in <em>dam</em>, <em>rep</em>, <em>rdgC</em>, <em>lexA</em>, or <em>polA</em>. Modulating the activity of the RecA recombinase partially suppressed the detrimental effects of <em>rdgC</em> or <em>lexA</em> mutations in Δ<em>priB</em> cells. Taken together, our results highlight roles for several genes in DSB homeostasis and define a genetic network that facilitates DNA repair/processing upstream of PriA/PriB-mediated DNA replication restart in <em>E. coli</em>.</p>
RBBP4 regulates the expression of Mre11-Rad50-NBS1(MRN)complex and promotes DNA double-strand breaks repair to mediate glioblastoma Chemoradiotherapy resistance
<p>Article <a>related</a> SUPPLEMENTARY data.</p> <p> </p>
Dynamic interplay of cNHEJ and MMEJ pathways of DNA double-strand break repair during embryonic development in zebrafish.
<p><span>Fastq sequences from zebrafish embryos corresponding to 9 amplicons sequenced by </span><span>Illumina MiSeq. DNA sample were obtained from non-treated wildtype controls (ctrl) or from wildtype (WT), polq mutants, lig3 mutant or lig4 mutant injected with Cas9 protein and a pool of 5 or 4 different sgRNA (numbered from 1#1 to 5#2). Each target site corresponds to one amplicon. </span></p>
Processed data from Repair-seq screens of double-strand breaks
<p>Processed data from Repair-seq screens of double-strand breaks induced by SpCas9 and AsCas12a in the presence or absence of oligonucleotide homology donors.</p>
Annotated DNA Double Strand Break Ionizing Radiation-Induced Foci (gH2AX 53BP1) Confocal Microscopy, pt. 2
<p><strong>Summary</strong></p> <p>Dataset of confocal microscopy data of cells exposed to gamma-irradiation and immunostained with gH2AX and 53BP1.</p> <ul> <li>Nuclei segmentation Head and neck primocultures immunostained with gH2AX/53BP1, Training/Testing/Validation dataset (nucleus_segmentation.zip) (available in part 1, <a href="https://dx.doi.org/10.5281/zenodo.4067741">https://dx.doi.org/10.5281/zenodo.4067741</a>) </li> <li>IRIF Foci: Head and neck primocultures immunostained with gH2AX/53BP1, Training/Testing/Validation dataset. (foci_detection.zip) (available in part 1, <a href="https://dx.doi.org/10.5281/zenodo.4067741">https://dx.doi.org/10.5281/zenodo.4067741</a>)</li> <li>Cell lines: U-87 and NHDF Cells exposed to 0.5-8 Gy 30 min and 8h post irradiation - confocal microscopy data of gH2AX/53BP1/DAPI annotated for gH2AX, 53BP1 and colocalized foci separately (cell_lines_U87.zip and cell_lines_NHDF.zip, this part of dataset) </li> <li><strong>Code</strong>: the code is available at <a href="https://github.com/tomasvicar/DeepFoci">https://github.com/tomasvicar/DeepFoci</a></li> <li><strong>Preprint: </strong>Vicar et al, DeepFoci: Deep Learning-Based Algorithm for Fast Automatic Analysis of DNA Double Strand Break Ionizing Radiation-Induced Foci, <a href="https://doi.org/10.1101/2020.10.07.321927">10.1101/2020.10.07.321927</a></li> <li><strong>Publication: </strong>Vicar et al, TBA</li> </ul> <p><strong>Materials and methods</strong></p> <p><em>Dataset</em></p> <p>Following cells were used:</p> <p>1) The training/validation/testing datasets was based on patient-derived primary cell cultures prepared from spinocellular tumors and morphologically normal tissues adjacent to the tumor taken from patients suffering from head and neck cancer. The dataset was divided into two subsets: one for training, validation and testing the nucleus segmentation (237/10/30 fields of view (FOVs), respectively) and one for training, validation and testing the focus segmentation (239/60/100 FOVs). The dataset consisted of several cell types: a) tumor cells, b) tumor-associated fibroblasts, and c) cells from morphologically normal tissues. All cell types were fixed at different periods of time (0 (non-irradiated control), 0.5, 8 or 24 h PI) after exposure to 2 Gy of gamma-rays. The representation of cells in two subsets with respect to the cell type and post-irradiation time (i.e., DSB repair duration) was random.</p> <p>2) The evaluation dataset was used to assess the robustness of segmentation procedures. It was composed of multiple types of differently treated cells in order to represent a highly challenging dataset maximally reflecting high biological and technical variability between samples, as it may appear in research or clinical practice. The dataset contained a) mesenchymal NHDF fibroblasts coming from a standard permanent cell line, b) radioresistant U-87 glioblastoma cells coming from a standard permanent cell line, c) tumor cells (CD90-) and tumor-associated fibroblasts (CD90+) prepared as a primary culture from a spinocellular tumors of patients (different from dataset 1) suffering from a head and neck cancer, and d) cells prepared as primary cultures from morphologically normal tissue adjacent to tumors of involved head and neck cancer patients. NHDF and U-87 cells received 0.5, 0, 1, 2, 4 and 8 Gy of gamma-rays and were fixed at 30 min and 8 h post-irradiation, while the primary cultures were only exposed to the dose of 2 Gy (for a limited amount of the cell material) and fixed at 0 (non-irradiated control), 0.5, 8 or 24 h post-irradiation times.</p> <p><em>Gamma irradiation</em></p> <p>The cells were irradiated at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic in a following schemes: (a) patient-derived primoculture was irradiated with a single dose of 2 Gy (D = 1 Gy/min) of gamma-rays (60Co, Chisostat, Chirana, CR) , (b) U-87 and NHDF cells were irradiated with doses 0.5-8 Gy (D = 1 Gy/min). Cells were irradiated in RPMI 1640 medium (37 °C, normal atmosphere). Confocal microscopy of gammaH2AX and 53BP1 foci immunodetection was consequently performed.</p> <p><em>Fluorescent staining</em></p> <p>DNA double strand breaks (DSBs) were quantified in different periods of time post-irradiation (30 min, 8h and 24h post irradiation) by means of $\gamma$H2AX and 53BP1 foci immunodetection combined with confocal microscopy. For details see \cite{falk2007chromatin}.</p> <p><em>Confocal microscopy</em></p> <p>The microscopy of samples was performed at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic. Leica DM RXA microscope (equipped with DMSTC motorized stage, Piezzo z-movement, MicroMax CCD camera, CSU-10 confocal unit and 488, 562, and 714 nm laser diodes with AOTF) was used for acquiring detailed cell images (100× oil immersion Plan Fluotar lens, NA 1.3). Total 50 Z slices was captured with Z step size 0.3 μm.</p> <p><strong>File description</strong></p> <p>all files are compressed hyperstack tiffs (50 Z slices and 3 fluorescent channels, XYCZ order), 100x magnification</p> <ul> <li>foci_detection.zip: IRIF Foci (available in part 1, <a href="https://dx.doi.org/10.5281/zenodo.4067741">https://dx.doi.org/10.5281/zenodo.4067741</a>): Head and neck primocultures immunostained with gH2AX/53BP1, Training/Testing/Validation dataset: FOVs 240/100/120 files for training, testing, and validation, organisation: <ul> <li>data_001.tif – 3channel Z.stack tiff</li> <li>mask_001.tif – respective Z stack mask with single points per IRIF focus (manual annotation, training and testing subsets only)</li> <li>data_description.xlsx – description of sample type (2Gy post irradiation times and characteristics of primary culture of squamous cell cancer of patients)</li> <li>data_001_pos.csv – manual annotation of gH2AX/53BPI IRIF foci by two experts – cordinates file (in 2D, validation only)</li> </ul> </li> <li>nucleus_segmentation.zip (available in part 1, <a href="https://dx.doi.org/10.5281/zenodo.4067741">https://dx.doi.org/10.5281/zenodo.4067741</a>) Nuclei segmentation Head and neck primocultures immunostained with gH2AX/53BP1, FOVs 237 Training/ 30 Testing/ 10 Validation dataset <ul> <li>data_001.tif – 3channel Z.stack tiff</li> <li>mask_001.tif – respective Z stack mask with manually annotated nucleus mask (manual annotation, training and testing subsets only)</li> <li>data_description.xlsx – description of sample type (2Gy post irradiation times and characteristics of primary culture of squamous cell cancer of patients)</li> </ul> </li> <li>U87.zip and NHDF.zip: Annotated gH2AX/53BP1 foci in cell lines exposed to increasing dose, annotations performed for gH2AX, 53BP1 and colocalized focus separatelly. 679 annotated FOVs for both cell lines. <ul> <li>control.png - RGB control figure showing merge and annotated overlay</li> <li>data_53BP1.tif - TIFF Z-stack, confocal microcopy, 53BP1 channel</li> <li>data_DAPI.tif - TIFF Z-stack, confocal microcopy, DAPI channel</li> <li>data_gH2AX.tif - TIFF Z-stack, confocal microcopy, gH2AX channel</li> <li>labels.json - foci labels for individual channel</li> <li>mask.tif - generated Z-stack of nucleus mask</li> </ul> </li> </ul>
Project files provided as supporting information to the manuscript "Kinetics of radiation-induced DNA double-strand breaks through coarse-grained simulations"
<p><strong>README file to the project files provided as supporting information to the manuscript “Kinetics of radiation-induced DNA double-strand breaks through coarse-grained simulations"</strong></p> <p>Authors: Manuel Micheloni, Lorenzo Petrolli, Gianluca Lattanzi and Raffaello Potestio<br> ==================================</p> <p>The .zip file is structured as follows:</p> <p>##############<br> 0_DNA_Sequence<br> ##############</p> <p>The folder contains:<br> • DNAsequence.txt: the DNA molecule employed in the study. <br> • ecseq.txt: the structure of the DNA. Each nucleotide (LAMMPS residue ID) is associated with the chemical type of the nucleic base.</p> <p>###################<br> 1_DSB_MDSimulations<br> ###################</p> <p>• MDSimulations: <br> The LAMMPS MD simulation scripts.<br> The subfolders are structured and named after different DSB motifs (folders 0,1, …,3) providing different external forces (folders 1000, 1100, 1200 refers to the respective average end-to-end distance). The latter subfolders provides:</p> <p>I. LMP_script provides the LAMMPS input file.</p> <p>II. the local internal energy contributions from the nucleotides involved with the residual contact interface between broken DNA moieties (data/1.E); </p> <p>III. coordinates of the nucleotides involved with the residual contact interface between the DNA moieties (data/2.POS);</p> <p>IV. the binary LAMMPS data file, employed as starting coordinates for the DSB MD simulation (/input_structure).</p> <p><br> • ScriptsAndAnalysis:<br> The scripts employed to analyze the DSB process. </p> <p>I. /00_GeneralScripts all the MATLAB functions employed for the analysis.</p> <p>II. /1_SigmoidalFitting provides the scripts from a sigmoidal fitting procedure [1] on the internal energy profile of the nucleotides between the strand breaks (Section 2 of the Supplementary Material). <br> [1] R P (2022). sigm_fit (https://www.mathworks.com/matlabcentral/fileexchange/42641-sigm_fit), MATLAB Central File Exchange. Retrieved July 2, 2022.</p> <p><br> ##################<br> 2_DNAFreeDiffusion<br> ##################</p> <p>• SIM:<br> It contains the MD simulations of the freely-diffusing DNA. Namely, the MSD of the DNA molecule, the input structure, and the LAMMPS simulation scripts are reported in /data, /input_structure, and /LMP_scripts respectively.</p> <p><br> • ANALYSIS:<br> It provides the script employed to estimate the diffusion coefficient of the DNA molecule and the time-scaling factor \Gamma(\zeta).</p> <p>#######################<br> 3_ForceAnalysis<br> #######################</p> <p>• data<br> It contains the forces computed from the MD simulations of the intact DNA molecules subject to the external force of 0.42, 0.88 and 3.06 pN. All data are stored in pickle format.<br> The README file contains additional information.</p> <p><br> NOTE1: Most data/scripts are saved according to the format .mat, employed by MATLAB Ⓡ, a numerical computing environment and proprietary programming language developed by MathWorks.</p> <p>NOTE2: For the force data manipulation, we acknowledge the use of LammpsFileManipulation package (https://pypi.org/project/LammpsFileManipulation/)</p>
Assessing Induction of Double Strand Breaks With Androgen Receptor Partial Agonist in Patients on Androgen Suppression
ClinicalTrials.gov study NCT03507608. IPD Sharing: NO. Countries: 1. Publications: 1.
Microscopy data from: Identification of genetic interactions with priB links the PriA/PriB DNA replication restart pathway to double-strand DNA break repair in Escherichia coli
Open the record for dataset details and reuse information.
Data from: Topological DNA-binding of SMC-like RecN promotes RecA-mediated DNA double-strand break repair
<p>Bacterial RecN, closely related to the structural maintenance of chromosomes (SMC) family of proteins, functions in the repair of DNA double-strand breaks (DSBs) by homologous recombination. However, the understanding of how RecN acts in concert with the RecA recombinase to promote DSB repair remains limited. Here, we demonstrated that the purified Escherichia coli RecN protein topologically loads onto both single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) that has a preference for ssDNA. RecN topologically bound to dsDNA slides off the end of linear dsDNA, but this is prevented by RecA nucleoprotein filaments on ssDNA, thereby allowing RecN to translocate to DSBs. Furthermore, we found that, once RecN is recruited onto ssDNA, it can topologically capture a second dsDNA substrate in an ATP-dependent manner, suggesting a role in synapsis. Indeed, RecN stimulates RecA-mediated D-loop formation and subsequent strand exchange activities. Our findings provide mechanistic insights into the recruitment of RecN to DSBs and sister chromatid interactions by RecN, both of which function in RecA-mediated DSB repair.</p>
DNA Double-strand Breaks After SPECT
ClinicalTrials.gov study NCT01380821. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data from: Topological DNA-binding of SMC-like RecN promotes RecA-mediated DNA double-strand break repair
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Data from: Meiotic double strand DNA breaks and spontaneous mutation in <em>Drosophila melanogaster</em>
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Data from: Rev7 and 53BP1/Crb2 prevent RecQ helicase-dependent hyper-resection of DNA double-strand breaks
Poly(ADP ribose) polymerase inhibitors (PARPi) target cancer cells deficient in homology-directed repair of DNA double-strand breaks (DSBs). In preclinical models, PARPi resistance is tied to altered nucleolytic processing (resection) at the 5' ends of a DSB. For example, loss of 53BP1 or Rev7/MAD2L2/FANCV derepresses resection to drive PARPi resistance, although the mechanisms are poorly understood. Long-range resection can be catalyzed by two machineries: the exonuclease Exo1, or the combination of a RecQ helicase and Dna2. Here, we develop a single cell microscopy assay that allows the distinct phases and machineries of resection to be interrogated simultaneously in living S. pombe cells. Using this assay, we find that the 53BP1 orthologue and Rev7 specifically repress long-range resection through the RecQ helicase-dependent pathway, thereby preventing hyper-resection. These results suggest that 'rewiring' of BRCA1-deficient cells to employ an Exo1-independent hyper-resection pathway is a driver of PARPi resistance.
Data from: Down-regulation of Rad51 activity during meiosis in yeast prevents competition with Dmc1 for repair of double-strand breaks
Interhomolog recombination plays a critical role in promoting proper meiotic chromosome segregation but a mechanistic understanding of this process is far from complete. In vegetative cells, Rad51 is a highly conserved recombinase that exhibits a preference for repairing double strand breaks (DSBs) using sister chromatids, in contrast to the conserved, meiosis-specific recombinase, Dmc1, which preferentially repairs programmed DSBs using homologs. Despite the different preferences for repair templates, both Rad51 and Dmc1 are required for interhomolog recombination during meiosis. This paradox has recently been explained by the finding that Rad51 protein, but not its strand exchange activity, promotes Dmc1 function in budding yeast. Rad51 activity is inhibited in dmc1Δ mutants, where the failure to repair meiotic DSBs triggers the meiotic recombination checkpoint, resulting in prophase arrest. The question remains whether inhibition of Rad51 activity is important during wild-type meiosis, or whether inactivation of Rad51 occurs only as a result of the absence of DMC1 or checkpoint activation. This work shows that strains in which mechanisms that down-regulate Rad51 activity are removed exhibit reduced numbers of interhomolog crossovers and noncrossovers. A hypomorphic mutant, dmc1-T159A, makes less stable presynaptic filaments but is still able to mediate strand exchange and interact with accessory factors. Combining dmc1-T159A with up-regulated Rad51 activity reduces interhomolog recombination and spore viability, while increasing intersister joint molecule formation. These results support the idea that down-regulation of Rad51 activity is important during meiosis to prevent Rad51 from competing with Dmc1 for repair of meiotic DSBs.
Annotated DNA Double Strand Break Ionizing Radiation-Induced Foci (gH2AX 53BP1) Confocal Microscopy, pt. 1
<p><strong>Summary</strong></p> <p>Dataset of confocal microscopy data of cells exposed to gamma-irradiation and immunostained with gH2AX and 53BP1.</p> <ul> <li>Nuclei segmentation Head and neck primocultures immunostained with gH2AX/53BP1, Training/Testing/Validation dataset (nucleus_segmentation.zip)</li> <li>IRIF Foci: Head and neck primocultures immunostained with gH2AX/53BP1, Training/Testing/Validation dataset. (foci_detection.zip)</li> <li>Cell lines: U-87 and NHDF Cells exposed to 0.5-8 Gy 30 min and 8h post irradiation - confocal microscopy data of gH2AX/53BP1/DAPI annotated for gH2AX, 53BP1 and colocalized foci separately (cell_lines_U87.zip and NHDF.zip part 2 of dataset, available at <a href="https://dx.doi.org/10.5281/zenodo.5549971">10.5281/zenodo.5549971</a>). </li> <li><strong>Code</strong>: the code is available at <a href="https://github.com/tomasvicar/DeepFoci">https://github.com/tomasvicar/DeepFoci</a></li> <li><strong>Preprint: </strong>Vicar et al, DeepFoci: Deep Learning-Based Algorithm for Fast Automatic Analysis of DNA Double Strand Break Ionizing Radiation-Induced Foci, <a href="https://doi.org/10.1101/2020.10.07.321927">10.1101/2020.10.07.321927</a></li> <li><strong>Publication: </strong>Vicar et al, TBA</li> </ul> <p><strong>Materials and methods</strong></p> <p><em>Dataset</em></p> <p>Following cells were used:</p> <p>1) The training/validation/testing datasets was based on patient-derived primary cell cultures prepared from spinocellular tumors and morphologically normal tissues adjacent to the tumor taken from patients suffering from head and neck cancer. The dataset was divided into two subsets: one for training, validation and testing the nucleus segmentation (237/10/30 fields of view (FOVs), respectively) and one for training, validation and testing the focus segmentation (239/60/100 FOVs). The dataset consisted of several cell types: a) tumor cells, b) tumor-associated fibroblasts, and c) cells from morphologically normal tissues. All cell types were fixed at different periods of time (0 (non-irradiated control), 0.5, 8 or 24 h PI) after exposure to 2 Gy of gamma-rays. The representation of cells in two subsets with respect to the cell type and post-irradiation time (i.e., DSB repair duration) was random.</p> <p>2) The evaluation dataset was used to assess the robustness of segmentation procedures. It was composed of multiple types of differently treated cells in order to represent a highly challenging dataset maximally reflecting high biological and technical variability between samples, as it may appear in research or clinical practice. The dataset contained a) mesenchymal NHDF fibroblasts coming from a standard permanent cell line, b) radioresistant U-87 glioblastoma cells coming from a standard permanent cell line, c) tumor cells (CD90-) and tumor-associated fibroblasts (CD90+) prepared as a primary culture from a spinocellular tumors of patients (different from dataset 1) suffering from a head and neck cancer, and d) cells prepared as primary cultures from morphologically normal tissue adjacent to tumors of involved head and neck cancer patients. NHDF and U-87 cells received 0.5, 0, 1, 2, 4 and 8 Gy of gamma-rays and were fixed at 30 min and 8 h post-irradiation, while the primary cultures were only exposed to the dose of 2 Gy (for a limited amount of the cell material) and fixed at 0 (non-irradiated control), 0.5, 8 or 24 h post-irradiation times.</p> <p><em>Gamma irradiation</em></p> <p>The cells were irradiated at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic in a following schemes: (a) patient-derived primoculture was irradiated with a single dose of 2 Gy (D = 1 Gy/min) of gamma-rays (60Co, Chisostat, Chirana, CR) , (b) U-87 and NHDF cells were irradiated with doses 0.5-8 Gy (D = 1 Gy/min). Cells were irradiated in RPMI 1640 medium (37 °C, normal atmosphere). Confocal microscopy of gammaH2AX and 53BP1 foci immunodetection was consequently performed.</p> <p><em>Fluorescent staining</em></p> <p>DNA double strand breaks (DSBs) were quantified in different periods of time post-irradiation (30 min, 8h and 24h post irradiation) by means of $\gamma$H2AX and 53BP1 foci immunodetection combined with confocal microscopy. For details see \cite{falk2007chromatin}.</p> <p><em>Confocal microscopy</em></p> <p>The microscopy of samples was performed at the Institute of Biophysics, Czech Academy of Sciences, Brno, Czech Republic. Leica DM RXA microscope (equipped with DMSTC motorized stage, Piezzo z-movement, MicroMax CCD camera, CSU-10 confocal unit and 488, 562, and 714 nm laser diodes with AOTF) was used for acquiring detailed cell images (100× oil immersion Plan Fluotar lens, NA 1.3). Total 50 Z slices was captured with Z step size 0.3 μm.</p> <p><strong>File description</strong></p> <p>all files are compressed hyperstack tiffs (50 Z slices and 3 fluorescent channels, XYCZ order), 100x magnification</p> <ul> <li>foci_detection.zip: IRIF Foci: Head and neck primocultures immunostained with gH2AX/53BP1, Training/Testing/Validation dataset: FOVs 240/100/120 files for training, testing, and validation, organisation: <ul> <li>data_001.tif – 3channel Z.stack tiff</li> <li>mask_001.tif – respective Z stack mask with single points per IRIF focus (manual annotation, training and testing subsets only)</li> <li>data_description.xlsx – description of sample type (2Gy post irradiation times and characteristics of primary culture of squamous cell cancer of patients)</li> <li>data_001_pos.csv – manual annotation of gH2AX/53BPI IRIF foci by two experts – cordinates file (in 2D, validation only)</li> </ul> </li> <li>nucleus_segmentation.zip Nuclei segmentation Head and neck primocultures immunostained with gH2AX/53BP1, FOVs 237 Training/ 30 Testing/ 10 Validation dataset <ul> <li>data_001.tif – 3channel Z.stack tiff</li> <li>mask_001.tif – respective Z stack mask with manually annotated nucleus mask (manual annotation, training and testing subsets only)</li> <li>data_description.xlsx – description of sample type (2Gy post irradiation times and characteristics of primary culture of squamous cell cancer of patients)</li> </ul> </li> <li>U87.zip and NHDF.zip: Annotated gH2AX/53BP1 foci in cell lines exposed to increasing dose, annotations performed for gH2AX, 53BP1 and colocalized focus separatelly. 679 annotated FOVs for both cell lines (part 2 of dataset, available at <a href="https://dx.doi.org/10.5281/zenodo.5549971">10.5281/zenodo.5549971</a>). <ul> <li>control.png - RGB control figure showing merge and annotated overlay</li> <li>data_53BP1.tif - TIFF Z-stack, confocal microcopy, 53BP1 channel</li> <li>data_DAPI.tif - TIFF Z-stack, confocal microcopy, DAPI channel</li> <li>data_gH2AX.tif - TIFF Z-stack, confocal microcopy, gH2AX channel</li> <li>labels.json - foci labels for individual channel</li> <li>mask.tif - generated Z-stack of nucleus mask</li> </ul> </li> </ul>
Data from: The telomere bouquet is a hub where meiotic double-strand breaks, synapsis, and stable homolog juxtaposition are coordinated in the zebrafish, Danio rerio
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Data from: Rev7 and 53BP1/Crb2 prevent RecQ helicase-dependent hyper-resection of DNA double-strand breaks
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
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