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Marc Drolet

Researcher at Université de Montréal

Publications -  38
Citations -  1970

Marc Drolet is an academic researcher from Université de Montréal. The author has contributed to research in topics: DNA supercoil & Topoisomerase. The author has an hindex of 22, co-authored 36 publications receiving 1805 citations.

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Hypernegative Supercoiling Inhibits Growth by Causing RNA Degradation

TL;DR: A model by which hypernegative supercoiling inhibits growth is presented, in which the introduction of hypernegativesupercoiling by gyrase facilitates degradation of nascent RNA; overproduction of RNase HI limits the accumulation of hypernegatively supercoiled templates, thereby preventing extensive RNA degradation.
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Topoisomerases I and III inhibit R-loop formation to prevent unregulated replication in the chromosomal Ter region of Escherichia coli.

TL;DR: Next generation sequencing and qPCR for marker frequency analysis indicate that in E. coli type 1A topos are required to inhibit R-loop formation/accumulation mostly to prevent unregulated replication in Ter, and that they are essential to prevent excess negative supercoiling and its detrimental effects on cell growth and survival.
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Isolation of the topB gene encoding DNA topoisomerase III as a multicopy suppressor of topA null mutations in Escherichia coli.

TL;DR: It is shown that DNA topoisomerase III is able to relax transcription‐induced negative supercoiling both in vitro and in vivo, and it is found that R‐loop‐dependent hypernegativesupercoiling can be prevented by the activity of this topoisomersase in vivo.
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Roles of Type 1A Topoisomerases in Genome Maintenance in Escherichia coli

TL;DR: Bacterial type 1A topos maintain the stability of the genome by preventing over-replication originating from oriC and R-loops and by acting with RecQ, suggesting that RecQ acts with a type 2A topo on RecA-generated recombination intermediates.
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Depletion of RNase HI activity in Escherichia coli lacking DNA topoisomerase I leads to defects in DNA supercoiling and segregation

TL;DR: Data are revealed that RNase HI plays a more central role in DNA topology than previously thought, and the existence of a cellular response to loss of RNaseHI that counters the supercoiling activity of gyrase is revealed.