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Crucial role and mechanism of transcription-coupled DNA repair in bacteria
Integrated structure–function studies show that transcription-coupled DNA repair (TCR)—rather than global genomic repair—is responsible for most chromosomal repair events in bacteria, and that TCR mainly occurs independently of the Mfd translocase.
- Binod K. Bharati
- , Manjunath Gowder
- & Evgeny Nudler
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Article
| Open AccessSignatures of TOP1 transcription-associated mutagenesis in cancer and germline
Defective ribonucleotide excision repair causes ID4, an indel cancer signature characterized by deletions of 2–5 base pairs.
- Martin A. M. Reijns
- , David A. Parry
- & Andrew P. Jackson
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Pervasive lesion segregation shapes cancer genome evolution
Mutagenic lesions such as those that give rise to cancer frequently segregate—unrepaired—during cell division, resulting in phasing of multiple alleles across generations of daughter cells and consequent tumour heterogeneity.
- Sarah J. Aitken
- , Craig J. Anderson
- & Martin S. Taylor
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DNA damage detection in nucleosomes involves DNA register shifting
Cryo-electron microscopy structures reveal that the DNA-repair factor UV-DDB exposes inaccessible nucleosome lesions for binding by inducing a translational shift in the nucleosome position.
- Syota Matsumoto
- , Simone Cavadini
- & Nicolas H. Thomä
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Letter |
Structural basis for the initiation of eukaryotic transcription-coupled DNA repair
Cryo-electron microscopy analysis of yeast Rad26 bound to RNA polymerase II provides insight into the initiation of the transcription-coupled DNA repair mechanism in eukaryotes.
- Jun Xu
- , Indrajit Lahiri
- & Dong Wang
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Letter |
RNA m6A methylation regulates the ultraviolet-induced DNA damage response
Methylation at the 6 position of adenosine (m6A) in RNA is rapidly and transiently induced at DNA damage sites in response to ultraviolet irradiation.
- Yang Xiang
- , Benoit Laurent
- & Yang Shi
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Letter |
Nucleotide excision repair is impaired by binding of transcription factors to DNA
An analysis of cancer genomic data reveals an increased rate of somatic mutations at active transcription factor binding sites located both within promoter regions and distal from genes; the increased mutation rate at these genomic regions can be explained by reduced accessibility of the protein-bound DNA to nucleotide excision repair machinery.
- Radhakrishnan Sabarinathan
- , Loris Mularoni
- & Núria López-Bigas
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UvrD facilitates DNA repair by pulling RNA polymerase backwards
UvrD acts in nucleotide excision repair by using its helicase/translocase activity to induce RNA polymerase backtracking, enabling repair enzymes to access DNA lesions.
- Vitaly Epshtein
- , Venu Kamarthapu
- & Evgeny Nudler