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Darren D. Sledjeski

Researcher at University of Toledo Medical Center

Publications -  26
Citations -  2757

Darren D. Sledjeski is an academic researcher from University of Toledo Medical Center. The author has contributed to research in topics: Streptococcus pyogenes & rpoS. The author has an hindex of 19, co-authored 26 publications receiving 2708 citations. Previous affiliations of Darren D. Sledjeski include Ohio University & University of Toledo.

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DsrA RNA regulates translation of RpoS message by an anti-antisense mechanism, independent of its action as an antisilencer of transcription

TL;DR: It is proposed that DsrA pairing stimulates RpoS translation by acting as an anti-antisense RNA, freeing the translation initiation region from the cis-acting antisense RNA and allowing increased translation.
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The small RNA, DsrA, is essential for the low temperature expression of RpoS during exponential growth in Escherichia coli.

TL;DR: While RpoS expression is very low in exponential phase at temperatures of 30 degrees C and above, at 20 degrees C there is substantial synthesis of RPOS during exponential growth, all dependent on DsrA RNA, and dsrA expression is also increased at low temperatures.
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Hfq Is Necessary for Regulation by the Untranslated RNA DsrA

TL;DR: It is shown that an hfq mutant strain is defective for DsrA-mediated regulation of both rpoS and hns, and Hfq acts as a protein cofactor for the regulatory activities of D srA by either altering the structure of DSRA or forming an active RNA-protein complex.
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Escherichia coli Hfq has distinct interaction surfaces for DsrA, rpoS and poly(A) RNAs

TL;DR: The bacterial Sm-like protein Hfq facilitates RNA-RNA interactions involved in post-transcriptional regulation of the stress response and is explained how it can simultaneously bind a ncRNA and its mRNA target to facilitate the strand displacement reaction required for H fq-dependent translational regulation.
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A small RNA acts as an antisilencer of the H-NS-silenced rcsA gene of Escherichia coli.

TL;DR: It is found that the low level of expression from the rcsA promoter is due to transcriptional silencing by the histone-like protein H-NS; this silencing is sensitive to both sequence and context in a region upstream of the -35 region of the promoter.