Genomic Sites Ultrasensitive to Ultraviolet Radiation
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ABSTRACT:
PROVIDER: PRJNA564830 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:If the genome contains outlier sequences extraordinarily sensitive to environmental agents, these would be sentinels for monitoring personal carcinogen exposure and might drive direct changes in cell physiology rather than acting through rare mutations. New methods, adductSeq and freqSeq, provided statistical resolution to quantify rare lesions at single-base resolution across the genome. Primary human melanocytes, but not fibroblasts, carried spontaneous apurinic sites and TG sequence lesions more frequently than UV-induced cyclobutane pyrimidine dimers (CPDs). UV exposure revealed hyperhotspots acquiring CPDs up to 170 fold more frequently than the genomic average; these sites were more prevalent in melanocytes. Hyperhotspots were disproportionately located near genes, particularly for RNA-binding proteins, with the most-recurrent hyperhotspots at a fixed position within two motifs: one occurring at ETS1 transcription factor binding sites, known to be UV targets, and at sites of mTOR/TOP-tract translation regulation; the second occurring at A2-15TTCTY, which developed "dark CPDs" after UV exposure, repaired CPDs slowly, and had accumulated CPDs prior to the experiment. Motif locations active as hyperhotspots differed between cell types. Melanocyte CPD hyperhotspots aligned precisely with recurrent UV signature mutations in individual gene promoters of melanomas and with known cancer drivers. At sunburn levels of UV exposure, every cell would have a hyperhotspot CPD in each of the ~20 targeted cell pathways, making hyperhotspots act as epigenetic marks. Purpose: These experiments searched for genomic sites in human primary fibroblasts and melanocytes that are extraordinarily sensitive to DNA damage, primarily cyclobutane pyrimidine dimers (CPDs) induced by UVC or UVB radiation. They separately detected abasic sites and other spontaneous DNA damage when present.
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Project description:Kertinocyte cultures grown in 60 mm petri dishes were placed 186 mm from the solar simulator source (Solar-simulated ultraviolet radiation 1600W Xenon short arc lamp with an Oriel Air Mass 1 Direct Filter, (AM1:D:B; model 81074) and KG2 Short Pass Filter. irradiance 9.84 mW/cm² for UVA (98.3%), 0.174 mW/cm² for UVB (1.7%) and 10 mW/cm² (0.017 mW/cm² erythemally-weighted) for the total UVR irradiance) and received a dose of either 0, 10, 20 and 150 kJ/m2 of unweighted ultraviolet radiation and 0, 10 and 150 kJ/m2 of unweighted ultraviolet radiation with SPF 15 sunscreen filtration (Homosalate 3%, Octisalate 4%, Avobenzone 2%, Titanium dioxide 0.66%) (2 mg/cm2 sandwiched between two 5x5 inch quartz plates) and were temperature controlled at 37oC using a customized water-bath. Six and Twenty-four hours post-exposure cells were harvested and RNA was extracted and subjected to microarray analysis.
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2024-03-12 | E-MTAB-13832 | biostudies-arrayexpress
Project description:Ultraviolet (UV) radiation is a major source of skin damage. It is important to define the programmed gene expression change after UV exposure, particularly in the C57BL/6 lab mice model. Here we systematically analyze the acute gene expression change in mouse skin after UV exposure.
2021-08-21 | GSE182125 | GEO
Project description:Tumours most often arise from progression of precursor clones within a single anatomical niche. In the bone marrow, clonal progenitors can undergo malignant transformation to acute leukaemia, or differentiate into immune cells that contribute to disease pathology in peripheral tissues. Outside the marrow, these clones are potentially exposed to a variety of tissue-specific mutational processes, although the consequences of this are unclear. Here we investigate the development of blastic plasmacytoid dendritic cell neoplasm (BPDCN)-an unusual form of acute leukaemia that often presents with malignant cells isolated to the skin. Using tumour phylogenomics and single-cell transcriptomics with genotyping, we find that BPDCN arises from clonal (premalignant) haematopoietic precursors in the bone marrow. We observe that BPDCN skin tumours first develop at sun-exposed anatomical sites and are distinguished by clonally expanded mutations induced by ultraviolet (UV) radiation. A reconstruction of tumour phylogenies reveals that UV damage can precede the acquisition of alterations associated with malignant transformation, implicating sun exposure of plasmacytoid dendritic cells or committed precursors during BPDCN pathogenesis. Functionally, we find that loss-of-function mutations in Tet2, the most common premalignant alteration in BPDCN, confer resistance to UV-induced cell death in plasmacytoid, but not conventional, dendritic cells, suggesting a context-dependent tumour-suppressive role for TET2. These findings demonstrate how tissue-specific environmental exposures at distant anatomical sites can shape the evolution of premalignant clones to disseminated cancer.
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Project description:The 7SK/P-TEFb snRNP controls ultraviolet radiation-induced transcriptional reprogramming
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