The transcription fidelity factor GreA impedes DNA break repair

Priya Sivaramakrishnan, Leonardo A. Sepúlveda, Jennifer A. Halliday, Jingjing Liu, María Angélica Bravo Núñez, Ido Golding, Susan M. Rosenberg and Christophe Herman ()
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Priya Sivaramakrishnan: Baylor College of Medicine
Leonardo A. Sepúlveda: Baylor College of Medicine
Jennifer A. Halliday: Baylor College of Medicine
Jingjing Liu: Baylor College of Medicine
María Angélica Bravo Núñez: Baylor College of Medicine
Ido Golding: Baylor College of Medicine
Susan M. Rosenberg: Baylor College of Medicine
Christophe Herman: Baylor College of Medicine

Nature, 2017, vol. 550, issue 7675, 214-218

Abstract: Abstract Homologous recombination repairs DNA double-strand breaks and must function even on actively transcribed DNA. Because break repair prevents chromosome loss, the completion of repair is expected to outweigh the transcription of broken templates. However, the interplay between DNA break repair and transcription processivity is unclear. Here we show that the transcription factor GreA inhibits break repair in Escherichia coli. GreA restarts backtracked RNA polymerase and hence promotes transcription fidelity. We report that removal of GreA results in markedly enhanced break repair via the classic RecBCD–RecA pathway. Using a deep-sequencing method to measure chromosomal exonucleolytic degradation, we demonstrate that the absence of GreA limits RecBCD-mediated resection. Our findings suggest that increased RNA polymerase backtracking promotes break repair by instigating RecA loading by RecBCD, without the influence of canonical Chi signals. The idea that backtracked RNA polymerase can stimulate recombination presents a DNA transaction conundrum: a transcription fidelity factor that compromises genomic integrity.

Date: 2017
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DOI: 10.1038/nature23907

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