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Maureen K. Thomason

Researcher at University of Washington

Publications -  21
Citations -  1608

Maureen K. Thomason is an academic researcher from University of Washington. The author has contributed to research in topics: Listeria monocytogenes & RNA. The author has an hindex of 10, co-authored 19 publications receiving 1366 citations. Previous affiliations of Maureen K. Thomason include Georgetown University Medical Center & National Institutes of Health.

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Bacterial antisense RNAs: How many are there and what are they doing?

TL;DR: What is known about the functions and mechanisms of action for some of these antisense RNAs and important considerations for future research as well as potential applications are discussed.
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Global Transcriptional Start Site Mapping Using Differential RNA Sequencing Reveals Novel Antisense RNAs in Escherichia coli

TL;DR: A survey of the E. coli transcriptome carried out using a differential RNA sequencing approach, which can distinguish between primary and processed transcripts, and an automated prediction algorithm for transcriptional start sites (TSS), finding 14,868 TSS candidates, including 5,574 internal to annotated genes (iTSS) and 5,495 TSS corresponding to potential antisense RNAs (asRNAs).
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A small RNA that regulates motility and biofilm formation in response to changes in nutrient availability in Escherichia coli.

TL;DR: It is proposed that, in response to limited nutrient availability, increasing levels of McaS modulate steps in the progression to a sessile lifestyle.
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Genomic characterization of the Bacillus cereus sensu lato species: Backdrop to the evolution of Bacillus anthracis

TL;DR: The key genes required for Bacillus anthracis to cause anthrax have been acquired recently by horizontal gene transfer and its chromosome does not appear to be exceptional on a macroscopic scale compared with close relatives.
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Compensatory mutations improve general permissiveness to antibiotic resistance plasmids.

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.