Gene architecture is a determinant of the transcriptional response to bulky DNA damages.

Bulky DNA damages block transcription and compromise genome integrity and function. The cellular response to these damages includes global transcription shutdown. Still, active transcription is necessary for transcription-coupled repair and for induction of damage-response genes.

GENI: A web server to identify gene set enrichments in tumor samples.

The Cancer Genome Atlas (TCGA) and analogous projects have yielded invaluable tumor-associated genomic data. Despite several web-based platforms designed to enhance accessibility, certain analyses require prior bioinformatic expertise. To address this need, we developed Gene ENrichment Identifier (GENI, https://www.

Exons and introns exhibit transcriptional strand asymmetry of dinucleotide distribution, damage formation and DNA repair.

Recent cancer sequencing efforts have uncovered asymmetry in DNA damage induced mutagenesis between the transcribed and non-transcribed strands of genes. Here, we investigate the major type of damage induced by ultraviolet (UV) radiation, the cyclobutane pyrimidine dimers (CPDs), which are formed primarily in TT dinucleotides. We reveal that a transcriptional asymmetry already exists at the level of TT dinucleotide frequency and therefore also in CPD damage formation.

Publisher Correction: The cooperative action of CSB, CSA, and UVSSA target TFIIH to DNA damage-stalled RNA polymerase II.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

The cooperative action of CSB, CSA, and UVSSA target TFIIH to DNA damage-stalled RNA polymerase II.

The response to DNA damage-stalled RNA polymerase II (RNAPIIo) involves the assembly of the transcription-coupled repair (TCR) complex on actively transcribed strands. The function of the TCR proteins CSB, CSA and UVSSA and the manner in which the core DNA repair complex, including transcription factor IIH (TFIIH), is recruited are largely unknown. Here, we define the assembly mechanism of the TCR complex in human isogenic knockout cells.