Radhakrishnan Kanagaraj

Open AccessEditorial by John J. Murphy 1,*,†, Kalpana Surendranath 1,†,‡ and Radhakrishnan Kanagaraj 1,2,3,*,† 1 Genome Engineering Laboratory, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK 2 School of Life Sciences, University of Bedfordshire, Park Square, Luton LU1 3JU, UK 3 Centre for Drug Discovery and Development, Sathyabama Institute of Science and Technology, Chennai 600119, India * Authors to whom correspondence should be addressed.

Abstract Elevated levels of reactive oxygen species (ROS) reduce replication fork velocity by causing dissociation of the TIMELESS-TIPIN complex from the replisome. Here, we show that ROS generated by exposure of human cells to the ribonucleotide reductase inhibitor hydroxyurea (HU) promote replication fork reversal in a manner dependent on active transcription and formation of co-transcriptional RNA:DNA hybrids (R-loops).

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