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Nucleotide excision repair is a process that repairs damage to one strand of the DNA, particularly from UV irradiation, which distorts the DNA helix. The DNA flanking the damage site is cleaved to generate a single-stranded gap that is repaired by copying the undamaged strand to restore an intact helix.
Hereditary nucleotide excision repair deficiencies cause different cancerous and progeroid disorders of which the exact etiology is not understood. This study finds that prolonged binding of DNA repair factor TFIIH to DNA damage contributes to a more severe phenotype caused by DNA repair deficiency.
The antitumor drug trabectedin is more toxic to DNA-repair-proficient cells. Here the authors show that this is caused by persistent DNA breaks induced from an abortive repair reaction and develop “TRABI-Seq” to map the breaks to transcribed regions of the genome. Trabectedin may thus be used as a diagnostic and therapeutic in precision oncology.
Here the authors visualize the workings of ELOF1 in transcription-coupled DNA repair, showing that ELOF1 repositions repair factors on the surface of DNA damage-stalled RNA polymerase II to facilitate its ubiquitylation by the CRL4CSA E3 ligase and inactivation by UVSSA.
DNA damage repair is in the spotlight this year — the Nobel Prize in Chemistry 2015 was awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar “for mechanistic studies of DNA repair”.