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Article: Damage mapping techniques and the light they have shed on canonical and atypical UV photoproducts.

Bohm, Kaitlynne A / Wyrick, John J

2023 Volume 13, Page(s) 1102593

Abstract: Ultraviolet (UV) light is a pervasive threat to the DNA of terrestrial organisms. UV light induces helix-distorting DNA lesions, primarily cyclobutane pyrimidine dimers (CPDs) that form between neighboring pyrimidine bases. Unrepaired CPD lesions cause ... ...

Abstract	Ultraviolet (UV) light is a pervasive threat to the DNA of terrestrial organisms. UV light induces helix-distorting DNA lesions, primarily cyclobutane pyrimidine dimers (CPDs) that form between neighboring pyrimidine bases. Unrepaired CPD lesions cause cytosine-to-thymine (C>T) substitutions in dipyrimidine sequences, which is the predominant mutation class in skin cancer genomes. However, many driver mutations in melanoma (
Language	English
Publishing date	2023-01-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2022.1102593
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Article ; Online: Genome-wide impact of cytosine methylation and DNA sequence context on UV-induced CPD formation.

Wilson, Hannah E / Wyrick, John J

Environmental and molecular mutagenesis

2023 Volume 65 Suppl 1, Page(s) 14–24

Abstract: Exposure to ultraviolet (UV) light is the primary etiological agent for skin cancers because UV damages cellular DNA. The most frequent form of UV damage is the cyclobutane pyrimidine dimer (CPD), which consists of covalent linkages between neighboring ... ...

Abstract	Exposure to ultraviolet (UV) light is the primary etiological agent for skin cancers because UV damages cellular DNA. The most frequent form of UV damage is the cyclobutane pyrimidine dimer (CPD), which consists of covalent linkages between neighboring pyrimidine bases in DNA. In human cells, the 5' position of cytosine bases in CG dinucleotides is frequently methylated, and methylated cytosines in the TP53 tumor suppressor are often sites of mutation hotspots in skin cancers. It has been argued that this is because cytosine methylation promotes UV-induced CPD formation; however, the effects of cytosine methylation on CPD formation are controversial, with conflicting results from previous studies. Here, we use a genome-wide method known as CPD-seq to map UVB- and UVC-induced CPDs across the yeast genome in the presence or absence in vitro methylation by the CpG methyltransferase M.SssI. Our data indicate that cytosine methylation increases UVB-induced CPD formation nearly 2-fold relative to unmethylated DNA, but the magnitude of induction depends on the flanking sequence context. Sequence contexts with a 5' guanine base (e.g., GCCG and GTCG) show the strongest induction due to cytosine methylation, potentially because these sequence contexts are less efficient at forming CPD lesions in the absence of methylation. We show that cytosine methylation also modulates UVC-induced CPD formation, albeit to a lesser extent than UVB. These findings can potentially reconcile previous studies, and define the impact of cytosine methylation on UV damage across a eukaryotic genome.
MeSH term(s)	Humans ; Pyrimidine Dimers/genetics ; Base Sequence ; DNA Damage ; DNA Methylation/genetics ; Cytosine ; DNA/genetics ; Ultraviolet Rays/adverse effects ; Skin Neoplasms/etiology
Chemical Substances	Pyrimidine Dimers ; Cytosine (8J337D1HZY) ; DNA (9007-49-2)
Language	English
Publishing date	2023-08-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.22569
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Article ; Online: Analysis of cytosine deamination events in excision repair sequencing reads reveals mechanisms of incision site selection in NER.

Morledge-Hampton, Benjamin / Kalyanaraman, Ananth / Wyrick, John J

Nucleic acids research

2024 Volume 52, Issue 4, Page(s) 1720–1735

Abstract: Nucleotide excision repair (NER) removes helix-distorting DNA lesions and is therefore critical for genome stability. During NER, DNA is unwound on either side of the lesion and excised, but the rules governing incision site selection, particularly in ... ...

Abstract	Nucleotide excision repair (NER) removes helix-distorting DNA lesions and is therefore critical for genome stability. During NER, DNA is unwound on either side of the lesion and excised, but the rules governing incision site selection, particularly in eukaryotic cells, are unclear. Excision repair-sequencing (XR-seq) sequences excised NER fragments, but analysis has been limited because the lesion location is unknown. Here, we exploit accelerated cytosine deamination rates in UV-induced CPD (cyclobutane pyrimidine dimer) lesions to precisely map their locations at C to T mismatches in XR-seq reads, revealing general and species-specific patterns of incision site selection during NER. Our data indicate that the 5' incision site occurs preferentially in HYV (i.e. not G; C/T; not T) sequence motifs, a pattern that can be explained by sequence preferences of the XPF-ERCC1 endonuclease. In contrast, the 3' incision site does not show strong sequence preferences, once truncated reads arising from mispriming events are excluded. Instead, the 3' incision is partially determined by the 5' incision site distance, indicating that the two incision events are coupled. Finally, our data reveal unique and coupled NER incision patterns at nucleosome boundaries. These findings reveal key principles governing NER incision site selection in eukaryotic cells.
MeSH term(s)	Cytosine/chemistry ; Deamination ; DNA Damage ; Excision Repair ; Eukaryotic Cells/chemistry
Chemical Substances	Cytosine (8J337D1HZY)
Language	English
Publishing date	2024-02-29
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkad1195
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Article ; Online: DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.

Selvam, Kathiresan / Wyrick, John J / Parra, Michael A

International journal of molecular sciences

2024 Volume 25, Issue 8

Abstract: DNA repair pathways play a critical role in genome stability, but in eukaryotic cells, they must operate to repair DNA lesions in the compact and tangled environment of chromatin. Previous studies have shown that the packaging of DNA into nucleosomes, ... ...

Abstract	DNA repair pathways play a critical role in genome stability, but in eukaryotic cells, they must operate to repair DNA lesions in the compact and tangled environment of chromatin. Previous studies have shown that the packaging of DNA into nucleosomes, which form the basic building block of chromatin, has a profound impact on DNA repair. In this review, we discuss the principles and mechanisms governing DNA repair in chromatin. We focus on the role of histone post-translational modifications (PTMs) in repair, as well as the molecular mechanisms by which histone mutants affect cellular sensitivity to DNA damage agents and repair activity in chromatin. Importantly, these mechanisms are thought to significantly impact somatic mutation rates in human cancers and potentially contribute to carcinogenesis and other human diseases. For example, a number of the histone mutants studied primarily in yeast have been identified as candidate oncohistone mutations in different cancers. This review highlights these connections and discusses the potential importance of DNA repair in chromatin to human health.
MeSH term(s)	DNA Repair ; Nucleosomes/metabolism ; Nucleosomes/genetics ; Humans ; Histones/metabolism ; Histones/genetics ; Protein Processing, Post-Translational ; Mutation ; Animals ; DNA Damage ; Neoplasms/genetics ; Neoplasms/metabolism ; Histone Code ; Chromatin/metabolism ; Chromatin/genetics
Chemical Substances	Nucleosomes ; Histones ; Chromatin
Language	English
Publishing date	2024-04-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25084393
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Article ; Online: A half century of exploring DNA excision repair in chromatin.

Smerdon, Michael J / Wyrick, John J / Delaney, Sarah

The Journal of biological chemistry

2023 Volume 299, Issue 9, Page(s) 105118

Abstract: DNA in eukaryotic cells is packaged into the compact and dynamic structure of chromatin. This packaging is a double-edged sword for DNA repair and genomic stability. Chromatin restricts the access of repair proteins to DNA lesions embedded in nucleosomes ...

Abstract	DNA in eukaryotic cells is packaged into the compact and dynamic structure of chromatin. This packaging is a double-edged sword for DNA repair and genomic stability. Chromatin restricts the access of repair proteins to DNA lesions embedded in nucleosomes and higher order chromatin structures. However, chromatin also serves as a signaling platform in which post-translational modifications of histones and other chromatin-bound proteins promote lesion recognition and repair. Similarly, chromatin modulates the formation of DNA damage, promoting or suppressing lesion formation depending on the chromatin context. Therefore, the modulation of DNA damage and its repair in chromatin is crucial to our understanding of the fate of potentially mutagenic and carcinogenic lesions in DNA. Here, we survey many of the landmark findings on DNA damage and repair in chromatin over the last 50 years (i.e., since the beginning of this field), focusing on excision repair, the first repair mechanism studied in the chromatin landscape. For example, we highlight how the impact of chromatin on these processes explains the distinct patterns of somatic mutations observed in cancer genomes.
MeSH term(s)	Chromatin/genetics ; DNA/metabolism ; DNA Damage ; Excision Repair ; Nucleosomes/genetics
Chemical Substances	Chromatin ; DNA (9007-49-2) ; Nucleosomes
Language	English
Publishing date	2023-07-30
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.105118
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Article ; Online: Genome-Wide Mapping of UV-Induced DNA Damage with CPD-Seq.

Mao, Peng / Wyrick, John J

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2175, Page(s) 79–94

Abstract: Exposure to ultraviolet (UV) radiation is the major risk factor for skin cancers. UV induces helix-distorting DNA damage such as cyclobutane pyrimidine dimers (CPDs). If not repaired, CPDs can strongly block DNA and RNA polymerases and cause mutagenesis ... ...

Abstract	Exposure to ultraviolet (UV) radiation is the major risk factor for skin cancers. UV induces helix-distorting DNA damage such as cyclobutane pyrimidine dimers (CPDs). If not repaired, CPDs can strongly block DNA and RNA polymerases and cause mutagenesis or cell death. Nucleotide excision repair (NER) is critical for the removal of UV-induced photolesions including CPDs in the cell. Investigating CPD formation and repair across the genome is important for understanding the mechanisms by which these lesions promote somatic mutations in skin cancers. Here we describe a high-throughput, single nucleotide-resolution damage mapping method named CPD sequencing (CPD-seq) for genome-wide analysis of UV-induced CPDs. Protocols for CPD-seq library preparation in yeast and human cells, as well as bioinformatics identification of the CPD damage site, are detailed below.
MeSH term(s)	Cell Line ; Chromosome Mapping/methods ; Computational Biology ; DNA Damage/radiation effects ; Fibroblasts/radiation effects ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Pyrimidine Dimers/genetics ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/radiation effects ; Skin Neoplasms/genetics ; Ultraviolet Rays
Chemical Substances	Pyrimidine Dimers
Language	English
Publishing date	2021-11-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0763-3_7
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Article ; Online: Detecting recurrent passenger mutations in melanoma by targeted UV damage sequencing.

Selvam, Kathiresan / Sivapragasam, Smitha / Poon, Gregory M K / Wyrick, John J

Nature communications

2023 Volume 14, Issue 1, Page(s) 2702

Abstract: Sequencing of melanomas has identified hundreds of recurrent mutations in both coding and non-coding DNA. These include a number of well-characterized oncogenic driver mutations, such as coding mutations in the BRAF and NRAS oncogenes, and non-coding ... ...

Abstract	Sequencing of melanomas has identified hundreds of recurrent mutations in both coding and non-coding DNA. These include a number of well-characterized oncogenic driver mutations, such as coding mutations in the BRAF and NRAS oncogenes, and non-coding mutations in the promoter of telomerase reverse transcriptase (TERT). However, the molecular etiology and significance of most of these mutations is unknown. Here, we use a new method known as CPD-capture-seq to map UV-induced cyclobutane pyrimidine dimers (CPDs) with high sequencing depth and single nucleotide resolution at sites of recurrent mutations in melanoma. Our data reveal that many previously identified drivers and other recurrent mutations in melanoma occur at CPD hotspots in UV-irradiated melanocytes, often associated with an overlapping binding site of an E26 transformation-specific (ETS) transcription factor. In contrast, recurrent mutations in the promoters of a number of known or suspected cancer genes are not associated with elevated CPD levels. Our data indicate that a subset of recurrent protein-coding mutations are also likely caused by ETS-induced CPD hotspots. This analysis indicates that ETS proteins profoundly shape the mutation landscape of melanoma and reveals a method for distinguishing potential driver mutations from passenger mutations whose recurrence is due to elevated UV damage.
MeSH term(s)	Humans ; Melanoma/genetics ; Melanoma/metabolism ; Mutation ; Pyrimidine Dimers/genetics ; DNA Damage ; Melanocytes/metabolism ; Ultraviolet Rays/adverse effects ; Skin Neoplasms/genetics
Chemical Substances	Pyrimidine Dimers
Language	English
Publishing date	2023-05-11
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38265-3
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Article: Tips, Tricks, and Potential Pitfalls of CRISPR Genome Editing in

Antony, Jacob S / Hinz, John M / Wyrick, John J

Frontiers in bioengineering and biotechnology

2022 Volume 10, Page(s) 924914

Abstract: The versatility of clustered regularly interspaced short palindromic repeat (CRISPR)-associated (Cas) genome editing makes it a popular tool for many research and biotechnology applications. Recent advancements in genome editing in eukaryotic organisms, ... ...

Abstract	The versatility of clustered regularly interspaced short palindromic repeat (CRISPR)-associated (Cas) genome editing makes it a popular tool for many research and biotechnology applications. Recent advancements in genome editing in eukaryotic organisms, like fungi, allow for precise manipulation of genetic information and fine-tuned control of gene expression. Here, we provide an overview of CRISPR genome editing technologies in yeast, with a particular focus on
Language	English
Publishing date	2022-05-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2719493-0
ISSN	2296-4185
ISSN	2296-4185
DOI	10.3389/fbioe.2022.924914
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Article: Molecular mechanism of UV damage modulation in nucleosomes.

Stark, Bastian / Poon, Gregory M K / Wyrick, John J

Computational and structural biotechnology journal

2022 Volume 20, Page(s) 5393–5400

Abstract: Exposure to ultraviolet (UV) light causes the formation of mutagenic cyclobutane pyrimidine dimers (CPDs) in cellular DNA. Previous studies have revealed that CPD formation in nucleosomes, the building blocks of chromatin, shows a striking ∼10 base pair ( ...

Abstract	Exposure to ultraviolet (UV) light causes the formation of mutagenic cyclobutane pyrimidine dimers (CPDs) in cellular DNA. Previous studies have revealed that CPD formation in nucleosomes, the building blocks of chromatin, shows a striking ∼10 base pair (bp) periodic pattern. CPD formation is suppressed at positions where the DNA minor groove faces toward the histone octamer (minor-in) and elevated CPD formation at positions where the minor groove faces away from the histone octamer (minor-out). However, the molecular mechanism underlying this nucleosome photofootprint is unclear. Here, we analyzed ∼180 high-resolution nucleosome structures to characterize whether differences in DNA mobility or conformation are responsible for the CPD modulation in nucleosomes. Our results indicate that differences in DNA mobility cannot explain CPD modulation in nucleosome. Instead, we find that the sharp DNA bending around the histone octamer results in DNA conformations with structural parameters more susceptible to UV damage formation at minor-out positions and more resistant to CPD formation at minor-in positions. This analysis reveals the molecular mechanism responsible for periodic modulation of CPD formation and UV mutagenesis in nucleosomal DNA.
Language	English
Publishing date	2022-09-14
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2694435-2
ISSN	2001-0370
ISSN	2001-0370
DOI	10.1016/j.csbj.2022.08.071
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Article: Mutperiod: Analysis of periodic mutation rates in nucleosomes

Morledge-Hampton, Benjamin / Wyrick, John J.

Computational and Structural Biotechnology Journal. 2021, v. 19

2021

Abstract: Nucleosomes modulate DNA damage and repair, resulting in periodic mutation rates in nucleosomal DNA. Previous research has characterized these patterns in many sequenced tumor genomes; however, computational tools to identify and quantify these ... ...

Abstract	Nucleosomes modulate DNA damage and repair, resulting in periodic mutation rates in nucleosomal DNA. Previous research has characterized these patterns in many sequenced tumor genomes; however, computational tools to identify and quantify these periodicities have not been developed for the broader scientific community. Here, we describe mutperiod, a Python and R based toolset that quantifies nucleosome mutational periodicities and compares them across different genetic and cellular backgrounds. We use mutperiod to demonstrate that DNA mismatch repair contributes to the nucleosome mutational periodicity observed in esophageal adenocarcinomas, and that the strength of this mutational periodicity varies in different chromatin states.
Keywords	DNA ; DNA damage ; DNA repair ; adenocarcinoma ; biotechnology ; genome ; nucleosomes ; periodicity
Language	English
Size	p. 4177-4183.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	2694435-2
ISSN	2001-0370
ISSN	2001-0370
DOI	10.1016/j.csbj.2021.07.025
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