H
Houra Merrikh
Researcher at Vanderbilt University
Publications - 52
Citations - 2046
Houra Merrikh is an academic researcher from Vanderbilt University. The author has contributed to research in topics: DNA replication & Gene. The author has an hindex of 22, co-authored 43 publications receiving 1623 citations. Previous affiliations of Houra Merrikh include Massachusetts Institute of Technology & University of Washington.
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Journal ArticleDOI
Replication-transcription conflicts in bacteria
TL;DR: Findings are summarized which shed light on the significance of the problem and on how bacterial cells deal with unwanted encounters between the replication and transcription machineries.
Journal ArticleDOI
Replication-Transcription Conflicts Generate R-Loops that Orchestrate Bacterial Stress Survival and Pathogenesis
Kevin S. Lang,Ashley N. Hall,Christopher N. Merrikh,Mark N. Ragheb,Hannah Tabakh,Alex J. Pollock,Joshua J. Woodward,Julia E. Dreifus,Houra Merrikh +8 more
TL;DR: It is shown that pervasive R-loop formation at head-on collision regions completely blocks replication, elevates mutagenesis, and inhibits gene expression, and that the resolution of these structures is critical for bacterial stress survival and pathogenesis.
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Co-directional replication–transcription conflicts lead to replication restart
TL;DR: In vivo, co-directional transcription can disrupt replication, leading to the involvement of replication restart proteins, and in contrast to the findings in vitro, the replication restart machinery is involved in vivo in resolving potentially deleterious encounters due to head-on and co- Directional conflicts.
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Compensatory mutations improve general permissiveness to antibiotic resistance plasmids.
Wesley Loftie-Eaton,Kelsie Bashford,Hannah Quinn,Kieran Dong,Jack Millstein,Samuel S. Hunter,Maureen K. Thomason,Houra Merrikh,José Miguel Ponciano,Eva M. Top +9 more
TL;DR: The authors show that when bacteria adapt to one plasmid, they become generally permissive to plasmids carriage, and suggest that poor plasmID persistence can be caused by a high cost involving helicase–plasmid interactions that can be rapidly ameliorated.
Journal ArticleDOI
Inhibiting the Evolution of Antibiotic Resistance.
Mark N. Ragheb,Maureen K. Thomason,Chris Hsu,Patrick Nugent,John Gage,Ariana Nakta Samadpour,Ankunda Kariisa,Christopher N. Merrikh,Samuel I. Miller,David R. Sherman,David R. Sherman,Houra Merrikh +11 more
TL;DR: It is suggested that AMR development can be inhibited through inactivation of evolvability factors (potentially with “anti-evolution” drugs)—in particular, Mfd—providing an unexplored route toward battling the AMR crisis.