Language
English
Publication Date
1-1-2025
Journal
FEBS Letters
DOI
10.1002/1873-3468.15063
PMID
39582266
PMCID
PMC13296718
PubMedCentral® Posted Date
6-26-2026
PubMedCentral® Full Text Version
Author MSS
Abstract
DNA replication and RNA transcription processes compete for the same DNA template and, thus, frequently collide. These transcription-replication collisions are thought to lead to genomic instability, which places a selective pressure on organisms to avoid them. Here, we review the predisposing causes, molecular mechanisms, and downstream consequences of transcription-replication collisions (TRCs) with a strong emphasis on prokaryotic model systems, before contrasting prokaryotic findings with cases in eukaryotic systems. Current research points to genomic structure as the primary determinant of steady-state TRC levels and RNA polymerase regulation as the primary inducer of excess TRCs. We review the proposed mechanisms of TRC-induced DNA damage, attempting to clarify their mechanistic requirements. Finally, we discuss what drives genomes to select against TRCs.
Keywords
DNA Damage, DNA Replication, Transcription, Genetic, DNA-Directed RNA Polymerases, Humans, Genomic Instability, DNA repair, DNA replication, mutagenesis, replisome, RNA transcription, RNAP backtracking, transcription–replication collision
Published Open-Access
yes
Recommended Citation
Matthew B Cooke, Christophe Herman, and Priya Sivaramakrishnan, "Clues to Transcription/Replication Collision-Induced DNA Damage: It Was RNAP, in the Chromosome, With the Fork" (2025). Faculty, Staff and Students Publications. 6999.
https://digitalcommons.library.tmc.edu/baylor_docs/6999