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Sicyoidochytrium minutum DNA virus strain:Ns-Ss

ABSTRACT: Draft genome sequence of SmDNAV Ns-Ss

PROVIDER: PRJDB12391 | ENA |

REPOSITORIES: ENA

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Sicyoidochytrium minutum DNA virus strain:Nm-Ss

Project description:Draft genome sequence of SmDNAV Nm-Ss

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Project description:Sicyoidochytrium minutum DNA virus strain 001 (SmDNAV 001) is a double-stranded DNA (dsDNA) virus that infects the marine fungoid protist Sicyoidochytrium minutum. We report the draft genome sequence of SmDNAV 001. The 236,345-bp genome contained 358 coding sequences (CDSs) and 3 tRNA-coding sequences.

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Transcription profiling of Atlantic salmon gill epithelium from three different stocks migrating from freshwater river to lake (Saimaa stock, SS), brackish water (Neva stock, NS) or seawater (Teno stock, TS) were compared at three successive developmental stages (parr, smolt and postsmolt)

Project description:Transcripts of the gill epithelium from three different stocks of Atlantic salmon (Salmo salar) migrating from freshwater river to lake (Saimaa stock, SS), brackish water (Neva stock, NS) or seawater (Teno stock, TS) were compared at three successive developmental stages (parr, smolt and postsmolt) using the 16K GRASP cDNA microarray platform.

2010-06-01 | E-MEXP-2210 | biostudies-arrayexpress

RfaH counter-silences inhibition of transcript elongation by H-NS–StpA H-NS nucleoprotein filaments in pathogenic E. coli

Project description:Expression of virulence genes in pathogenic E. coli is controlled in part by the transcription silencer H-NS and its paralogs (e.g., StpA), which sequester DNA in multi-kb nucleoprotein filaments to inhibit transcription initiation, elongation, or both. Some activators counter-silence initiation by displacing H-NS from promoters. How H-NS inhibition of elongation is overcome is not understood. In uropathogenic E. coli (UPEC), elongation regulator RfaH aids expression of some H-NS-silenced pathogenicity operons (e.g., hlyCABD encoding hemolysin). RfaH associates with elongation complexes (ECs) via direct contacts to a transiently exposed, nontemplate DNA-strand sequence called ops (operon polarity suppressor). RfaH–ops interactions establish long-lived RfaH–EC contacts that allow RfaH to recruit ribosomes to the nascent mRNA and to suppress transcriptional pausing and termination. Using ChIP-seq, we mapped the genome-scale distributions of RfaH, H-NS, StpA, RNA polymerase (RNAP), and σ70 in the UPEC strain CFT073. We identify 8 RfaH-activated operons, all of which were bound by H-NS and StpA. Four are new additions to the RfaH regulon. Deletion of RfaH caused premature termination whereas deletion of H-NS and StpA allowed elongation without RfaH. Thus, RfaH is an elongation counter-silencer of H-NS. Consistent with elongation counter-silencing, deletion of StpA alone decreased the effect of RfaH. StpA increases DNA bridging, which inhibits transcript elongation via topological constraints on RNAP. Residual RfaH effect when both H-NS and StpA were deleted was attributable to targeting of RfaH-regulated operons by a minor H-NS paralog, Hfp. These operons have evolved higher levels of H-NS–binding features, explaining minor-paralog targeting.

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Project description:Transcriptional profiling of squamous cell carcinoma of oral tongue, comparing p53 NS+ and p53 NS- tumors. Goal was to determine differentially expressed genes between them based on global gene expression.

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