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Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation

ABSTRACT: Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation

PROVIDER: PRJNA682535 | ENA |

REPOSITORIES: ENA

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Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [WGS]

Project description:Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [WGS]

| PRJNA681787 | ENA

Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [aCGH]

Project description:Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [aCGH]

| PRJNA682537 | ENA

Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [Hi-C]

Project description:Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [Hi-C]

| PRJNA681800 | ENA

Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [WGS]

Project description:In this study, we compared the genomic landscape of resistant cell line HaCaT/SM to its progenitor HaCaT in order to gain insights into genetic changes associated with continuous alkylation and oxidative stress. We established chromosome numbers by cytogenetics, analyzed DNA copy number changes by means of array CGH, employed the genome-wide chromosome conformation capture technique Hi-C to detect chromosomal translocations and defined mutational signatures based on whole genome sequencing data. We observed the SM-associated elimination of the initially prevailing hypotetraploid cell population in favor of a hyperdiploid one, which contrasts with previous observations that link polyploidization to increased tolerance and adaptability towards genotoxic stress. Furthermore, we observed an accumulation of chromosomal translocations, frequently flanked by DNA copy number changes, which indicates a high rate of DNA double strand break misrepair. HaCaT/SM-specific single nucleotide variants showed enrichment of C>A and T>A transversions and a lower rate of deaminated cytosines in the CpG dinucleotide context. Given the frequent use of HaCaT in toxicology this study provides a valuable data source with respect to the original genotype of HaCaT and the mutational signatures associated with chronic alkylation and oxidative stress.

2021-01-27 | GSE162401 | GEO

Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [aCGH]

2021-01-27 | GSE162645 | GEO

Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation [Hi-C]

2021-01-27 | GSE162388 | GEO

Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation.

Project description:Sulfur mustard (SM) is a chemical warfare agent that can damage DNA via alkylation and oxidative stress. Because of its genotoxicity, SM is cancerogenic and the progenitor of many chemotherapeutics. Previously, we developed an SM-resistant cell line via chronic exposure of the popular keratinocyte cell line HaCaT to increasing doses of SM over a period of 40 months. In this study, we compared the genomic landscape of the SM-resistant cell line HaCaT/SM to its sensitive parental line HaCaT in order to gain insights into genetic changes associated with continuous alkylation and oxidative stress. We established chromosome numbers by cytogenetics, analyzed DNA copy number changes by means of array Comparative Genomic Hybridization (array CGH), employed the genome-wide chromosome conformation capture technique Hi-C to detect chromosomal translocations, and derived mutational signatures by whole-genome sequencing. We observed that chronic SM exposure eliminated the initially prevailing hypotetraploid cell population in favor of a hyperdiploid one, which contrasts with previous observations that link polyploidization to increased tolerance and adaptability toward genotoxic stress. Furthermore, we observed an accumulation of chromosomal translocations, frequently flanked by DNA copy number changes, which indicates a high rate of DNA double-strand breaks and their misrepair. HaCaT/SM-specific single-nucleotide variants showed enrichment of C > A and T > A transversions and a lower rate of deaminated cytosines in the CpG dinucleotide context. Given the frequent use of HaCaT in toxicology, this study provides a valuable data source with respect to the original genotype of HaCaT and the mutational signatures associated with chronic alkylation and oxidative stress.

| S-EPMC7865644 | biostudies-literature

Genomic adaptation and mutational patterns in a HaCaT subline resistant to alkylating agents and ionizing radiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-27 | GSE162646 | GEO

Gene expression profile at single cell level of HaCaT cells exposed to ionizing radiation

Project description:HaCaT cell line is a kind of keratinocyte from human skin. We used single cell RNA sequencing (scRNA-seq) to analyze the influnce of fractionated 2 Gy or single 20 Gy irradiation on HaCaT cells.

2022-12-31 | GSE210170 | GEO

The impact of commonly used alkylating agents on artefactual peptide modification

Project description:Iodoacetamide is by far the most commonly used agent for alkylation of cysteine during sample preparation for proteomics. An alternative, 2-chloroacetamide, has been recently suggested to reduce the alkylation of residues other than cysteine, such as the N-terminus, Asp, Glu, Lys, Ser, Thr and Tyr. Here, we show that although 2-chloroacetamide reduces the level of off-target alkylation, it exhibits a range of adverse effects. The most significant of these was methionine oxidation, which increases to a maximum of 40% of all Met containing peptides compared to 2-5% with iodoacetamide. Increases were also observed for mono and dioxidised tryptophan. No additional differences between the alkylating reagents were observed for a range of other post-translational modifications and digestion parameters. The adverse impact of 2-chloroacetamide on methionine oxidation suggest it is not the ideal alkylating reagent for proteomics.

2017-08-16 | PXD007071 | Pride

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