Repair of UV damage in Halobacterium salinarum

2003 ◽  
Vol 31 (3) ◽  
pp. 694-698 ◽  
Author(s):  
S. McCready ◽  
L. Marcello
Keyword(s):  
Excision Repair ◽  
Halobacterium Salinarum ◽  
Uv Damage ◽  
Cyclobutane Pyrimidine Dimers ◽  
Repair Capacity ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision ◽  
Repair Mechanisms ◽  
Uv Photoproducts ◽  
Repair Genes

Halobacterium is one of the few known Archaea that tolerates high levels of sunlight in its natural environment. Photoreactivation is probably its most important strategy for surviving UV irradiation and we have shown that both of the major UV photoproducts, cyclobutane pyrimidine dimers (CPDs) and (6–4) photoproducts, can be very efficiently repaired by photoreactivation in this organism. There are two putative photolyase gene homologues in the published genome sequence of Halobacterium sp. NRC-1. We have made a mutant deleted in one of these, phr2, and confirmed that this gene codes for a CPD photolyase. (6–4) photoproducts are still photoreactivated in the mutant so we are currently establishing whether the other homologue, phr1, codes for a (6–4) photolyase. We have also demonstrated an excision repair capacity that operates in the absence of visible light but the nature of this pathway is not yet known. There is probably a bacteria-type excision-repair mechanism, since homologues of uvrA, uvrB, uvrC and uvrD have been identified in the Halobacterium genome. However, there are also homologues of eukaryotic nucleotide-excision-repair genes (Saccharomy cescerevisiae RAD3, RAD25 and RAD2) so there may be multiple repair mechanisms for UV damage in Halobacterium.

scholarly journals Repair-Independent Chromatin Assembly onto Active Ribosomal Genes in Yeast after UV Irradiation

2005 ◽  
Vol 25 (22) ◽  
pp. 9773-9783 ◽  
Author(s):  
Antonio Conconi ◽  
Michel Paquette ◽  
Deirdre Fahy ◽  
Vyacheslav A. Bespalov ◽  
Michael J. Smerdon
Keyword(s):  
Excision Repair ◽  
Ribosomal Genes ◽  
Chromatin Assembly ◽  
Original Structure ◽  
Open Chromatin ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision ◽  
Multiple Copies ◽  
Uv Photoproducts

ABSTRACT Chromatin rearrangements occur during repair of cyclobutane pyrimidine dimers (CPDs) by nucleotide excision repair (NER). Thereafter, the original structure must be restored to retain normal genomic functions. How NER proceeds through nonnucleosomal chromatin and how open chromatin is reestablished after repair are unknown. We analyzed NER in ribosomal genes (rDNA), which are present in multiple copies but only a fraction are actively transcribed and nonnucleosomal. We show that removal of CPDs is fast in the active rDNA and that chromatin reorganization occurs during NER. Furthermore, chromatin assembles on nonnucleosomal rDNA during the early events of NER but in the absence of DNA repair. The resumption of transcription after removal of CPDs correlates with the reappearance of nonnucleosomal chromatin. To date, only the passage of replication machinery was thought to package ribosomal genes in nucleosomes. In this report, we show that early events after formation of UV photoproducts in DNA also promote chromatin assembly.

scholarly journals Emerging Roles of Post-Translational Modifications in Nucleotide Excision Repair

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1466 ◽  
Author(s):  
Barbara N. Borsos ◽  
Hajnalka Majoros ◽  
Tibor Pankotai
Keyword(s):  
Nucleotide Excision Repair ◽  
Ubiquitin Ligase ◽  
Excision Repair ◽  
Fine Tuning ◽  
Genome Integrity ◽  
Repair Pathway ◽  
Cyclobutane Pyrimidine Dimers ◽  
Post Translational Modifications ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision

Nucleotide excision repair (NER) is a versatile DNA repair pathway which can be activated in response to a broad spectrum of UV-induced DNA damage, such as bulky adducts, including cyclobutane-pyrimidine dimers (CPDs) and 6–4 photoproducts (6–4PPs). Based on the genomic position of the lesion, two sub-pathways can be defined: (I) global genomic NER (GG-NER), involved in the ablation of damage throughout the whole genome regardless of the transcription activity of the damaged DNA locus, and (II) transcription-coupled NER (TC-NER), activated at DNA regions where RNAPII-mediated transcription takes place. These processes are tightly regulated by coordinated mechanisms, including post-translational modifications (PTMs). The fine-tuning modulation of the balance between the proteins, responsible for PTMs, is essential to maintain genome integrity and to prevent tumorigenesis. In this review, apart from the other substantial PTMs (SUMOylation, PARylation) related to NER, we principally focus on reversible ubiquitylation, which involves E3 ubiquitin ligase and deubiquitylase (DUB) enzymes responsible for the spatiotemporally precise regulation of NER.

scholarly journals Nucleotide excision repair by dual incisions in plants

2016 ◽  
Vol 113 (17) ◽  
pp. 4706-4710 ◽  
Author(s):  
Fazile Canturk ◽  
Muhammet Karaman ◽  
Christopher P. Selby ◽  
Michael G. Kemp ◽  
Gulnihal Kulaksiz-Erkmen ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Plant Genome ◽  
Cyclobutane Pyrimidine Dimers ◽  
Repair Gene ◽  
Phosphodiester Bonds ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision ◽  
Dual Incision

Plants use light for photosynthesis and for various signaling purposes. The UV wavelengths in sunlight also introduce DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts [(6-4)PPs] that must be repaired for the survival of the plant. Genome sequencing has revealed the presence of genes for both CPD and (6-4)PP photolyases, as well as genes for nucleotide excision repair in plants, such asArabidopsisand rice. Plant photolyases have been purified, characterized, and have been shown to play an important role in plant survival. In contrast, even though nucleotide excision repair gene homologs have been found in plants, the mechanism of nucleotide excision repair has not been investigated. Here we used the in vivo excision repair assay developed in our laboratory to demonstrate thatArabidopsisremoves CPDs and (6-4)PPs by a dual-incision mechanism that is essentially identical to the mechanism of dual incisions in humans and other eukaryotes, in which oligonucleotides with a mean length of 26–27 nucleotides are removed by incising ∼20 phosphodiester bonds 5′ and 5 phosphodiester bonds 3′ to the photoproduct.

scholarly journals Xeroderma Pigmentosum: Gene Variants and Splice Variants

Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1173
Author(s):  
Marie Christine Martens ◽  
Steffen Emmert ◽  
Lars Boeckmann
Keyword(s):  
Dna Damage ◽  
Xeroderma Pigmentosum ◽  
Splice Variants ◽  
Excision Repair ◽  
Genetic Disorder ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Damage Repair ◽  
Nucleotide Excision ◽  
Functional Relevance

The nucleotide excision repair (NER) is essential for the repair of ultraviolet (UV)-induced DNA damage, such as cyclobutane pyrimidine dimers (CPDs) and 6,4-pyrimidine-pyrimidone dimers (6,4-PPs). Alterations in genes of the NER can lead to DNA damage repair disorders such as Xeroderma pigmentosum (XP). XP is a rare autosomal recessive genetic disorder associated with UV-sensitivity and early onset of skin cancer. Recently, extensive research has been conducted on the functional relevance of splice variants and their relation to cancer. Here, we focus on the functional relevance of alternative splice variants of XP genes.

scholarly journals Bioinformatic Prediction of Ultraviolet Light Mutagenesis Sensitivity of Human Genes and a Method for Genetically Engineering UVB Resistance

2011 ◽  
Vol 10 ◽  
pp. CIN.S6670
Author(s):  
Kevin A. Lease ◽  
Chris Papageorgio
Keyword(s):  
Excision Repair ◽  
Uv Light ◽  
Light Exposure ◽  
Loss Of Function ◽  
Cyclobutane Pyrimidine Dimers ◽  
Protein Coding ◽  
Protein Coding Genes ◽  
Pyrimidine Dimers ◽  
Human Genes ◽  
Nucleotide Excision

Living on earth, we are exposed to ultraviolet (UV) light as part of the solar radiation. UVB spectrum light exposure contributes to the development of skin cancer by interacting with pyrimidine pairs to create lesions called cyclobutane pyrimidine dimers. If these lesions are not removed by nucleotide excision repair, they often give rise to C to T transition mutations. Based on these observations, a bioinformatics approach was used to predict the vulnerability of human protein coding genes to UVB induced loss of function mutations. This data was used to evaluate in depth those genes associated with malignant melanoma. In addition, we demonstrate a method of genetically engineering genes that significantly improves resistance to UVB loss of function mutations.

scholarly journals Rescue of cells from apoptosis increases DNA repair in UVB exposed cells: implications for the DNA damage response

2015 ◽  
Vol 4 (3) ◽  
pp. 725-738 ◽  
Author(s):  
Mahsa Karbaschi ◽  
Salvador Macip ◽  
Vilas Mistry ◽  
Hussein H. K. Abbas ◽  
George J. Delinassios ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Nucleotide Excision Repair ◽  
Dna Damage Response ◽  
Excision Repair ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Nucleotide Excision ◽  
Damage Response ◽  
Lengthy Process

Classically, the nucleotide excision repair (NER) of cyclobutane pyrimidine dimers (CPD) is a lengthy process (t1/2 > 48 h).

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