Abstract
Genome replication involves dealing with obstacles that can result from DNA damage but also from chromatin alterations, topological stress, tightly bound proteins or non-B DNA structures such as R loops. Experimental evidence reveals that an engaged transcription machinery at the DNA can either enhance such obstacles or be an obstacle itself. Thus, transcription can become a potentially hazardous process promoting localized replication fork hindrance and stress, which would ultimately cause genome instability, a hallmark of cancer cells. Understanding the causes behind transcription–replication conflicts as well as how the cell resolves them to sustain genome integrity is the aim of this review.
Funder
European Research Council
Spanish Ministry of Economy and Competitiveness
Junta de Andalucía
Scientific Foundation of the Spanish Association Against Cancer
Publisher
Cold Spring Harbor Laboratory
Subject
Developmental Biology,Genetics
Cited by
166 articles.
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