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Transcriptional processing of G4 DNA
Author(s) -
Tornaletti Silvia
Publication year - 2009
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20513
Subject(s) - biology , transcription (linguistics) , genetics , genome instability , dna repair , nucleotide excision repair , dna , dna replication , gene , t cell receptor , dna re replication , computational biology , microbiology and biotechnology , dna damage , eukaryotic dna replication , t cell , philosophy , linguistics , immune system
Genomic DNA sequences with the ability to assume non‐B form secondary structures have been recently shown to be particularly susceptible to genetic instability, an early contributing factor in human disease and cancer development. Transcription appears to play a central role in formation of these structures and in promoting instability at these sites. The subpathway of nucleotide excision DNA repair, transcription‐coupled DNA repair (TCR), removes transcription‐arresting damage from the transcribed strands of expressed genes, but little is known about how non‐canonical DNA structures are processed when encountered by the transcription machinery. If such structures arrest transcription, they may elicit “gratuitous” TCR in which the resulting reiterative and futile repair replication might generate a significant level of mutagenesis in a frequently transcribed gene because of faulty processing in the area of transcription arrest. Here we will describe our current understanding of how TCR may be elicited at non‐B DNA structures and summarize recent literature describing the behavior of RNA polymerases when encountering non‐canonical DNA structures, with particular emphasis on quadruplex DNA. © 2009 Wiley‐Liss, Inc.