Publications by authors named "Dalton Plummer"
Article Synopsis
- UV light mainly causes C > T mutations in certain DNA sequences, but melanoma driver mutations often involve different changes like T > A, T > C, and C > A, which are not well understood in relation to UV exposure.
- Through experiments with yeast exposed to UVB and UVA light, researchers found that UVB mainly induces C > T, T > C, and T > A mutations, while UVA results in fewer mutations with a distinct pattern predominantly featuring C > A/G > T substitutions linked to oxidative damage.
- The study suggests that both UVB and UVA exposure can contribute to the noncanonical mutations associated with melanoma, with specific mechanisms and patterns underlying the mutations arising from each type of UV light.
UV exposure induces a mutation signature of C > T substitutions at dipyrimidines in skin cancers. We recently identified additional UV-induced AC > TT and A > T substitutions that could respectively cause BRAF V600K and V600E oncogenic mutations. The mutagenic bypass mechanism past these atypical lesions, however, is unknown.
View Article and Find Full Text PDFHelix-distorting DNA lesions, including ultraviolet (UV) light-induced damage, are repaired by the global genomic-nucleotide excision repair (GG-NER) and transcription coupled-nucleotide excision repair (TC-NER) pathways. Previous studies have shown that histone post-translational modifications (PTMs) such as histone acetylation and methylation can promote GG-NER in chromatin. Whether histone PTMs also regulate the repair of DNA lesions by the TC-NER pathway in transcribed DNA is unknown.
View Article and Find Full Text PDFCorrect transcription is crucial for life. However, DNA damage severely impedes elongating RNA polymerase II, causing transcription inhibition and transcription-replication conflicts. Cells are equipped with intricate mechanisms to counteract the severe consequence of these transcription-blocking lesions.
View Article and Find Full Text PDFNuA4 acetyltransferase is required for efficient nucleotide excision repair in yeast.
DNA Repair (Amst)
January 2019
The nucleotide excision repair (NER) pathway is critical for removing damage induced by ultraviolet (UV) light and other helix-distorting lesions from cellular DNA. While efficient NER is critical to avoid cell death and mutagenesis, NER activity is inhibited in chromatin due to the association of lesion-containing DNA with histone proteins. Histone acetylation has emerged as an important mechanism for facilitating NER in chromatin, particularly acetylation catalyzed by the Spt-Ada-Gcn5 acetyltransferase (SAGA); however, it is not known if other histone acetyltransferases (HATs) promote NER activity in chromatin.
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