Transcriptional mutagenesis and its potential roles in the etiology of cancer and bacterial antibiotic resistance. Issue 12 (23rd August 2013)

• Record Type: Journal Article
• Authors: Morreall, Jordan F.; Petrova, Lucy; Doetsch, Paul W.
• Is Part Of: Journal of cellular physiology. Volume 228:Issue 12(2013:Dec.)
• Page Start: 2257
• Page End: 2261
• Publication Date: 2013-08-23
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24400
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>ABSTRACT</title> <sec id="jcp24400-sec-0001" sec-type="section"> <p>Most cells do not undergo continuous cell division and DNA replication, yet they can still acquire novel RNA mutations that can result in the production of mutant proteins and induce a phenotypic change. All cells are frequently subjected to genotoxic insults that give rise to damaged nucleotides which, similarly to DNA replication, can undergo base mispairing during transcription. This mutagenic lesion bypass by RNA polymerase, transcriptional mutagenesis (TM), has been studied in a variety of systems and organisms, and may be involved in diverse pathogenic processes, such as tumorigenesis and the acquisition of bacterial antibiotic resistance. Tumor cells and bacteria within the human body are subject to especially high levels of oxidative stress, which can damage DNA and consequently drive TM. Mutagenesis at the level of transcription may allow cells to escape growth arrest and undergo replication that could permanently establish mutations in DNA in a process called retromutagenesis (RM). Here, we review the broad range of DNA damages which may result in TM including a variety of non‐bulky lesions and some bulky lesions, which recent studies indicate may not completely block transcription, and emerging evidence supporting the RM concept in the context of tumorigenesis and antibiotic resistance. J. Cell. Physiol. 228: 2257–2261, 2013. © 2013 Wiley Periodicals, Inc.</p> </sec> </abstract>