Enterococcus faecalis rpoN mutant gene expression changes
Ontology highlight
ABSTRACT:
ORGANISM(S): Enterococcus faecalis V583
PROVIDER: GSE40237 | GEO | 2018/08/10
REPOSITORIES: GEO
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Project description:Enterococcus faecalis rpoN mutant gene expression changes
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Project description:The enterococci comprise a genus of 49 low-GC content Gram-positive commensal species within the Firmicutes phylum that are known to occupy diverse habitats, notably the gastrointestinal core microbiota of nearly every phylum, including human. Of particular clinical relevance are two rogue species of enterococci, Enterococcus faecalis and the distantly related Enterococcus faecium, standing among the nefarious multi-drug resistant and hospital-acquired pathogens. Despite increasing evidence for RNA-based regulation in the enterococci, including regulation of virulence factors, their transcriptome structure and arsenal of regulatory small sRNAs (sRNAs) are not thoroughly understood. Using dRNA-seq, we have mapped at single-nucleotide resolution the primary transcriptomes of E. faecalis V583 and E. faecium AUS0004. We identified 2517 and 2771 transcription start sites (TSS) in E. faecalis and E. faecium, respectively. Based on the identified TSS, we created a global map of s70 promoter motifs. We also revealed features of 5’ and 3’UTRs across the genomes. The transcriptome maps also predicted 150 and 128 sRNA candidates in E. faecalis and E. faecium, respectively, some of which have been identified in previous studies and many of which are new. Finally, we validated several of the predicted sRNAs by Northern Blot in biologically relevant conditions. Comprehensive TSS mapping of two representative strains will provide a valuable resource for the continued development of RNA biology in the Enterococci.
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Project description:Experiment conducted to investigate the genetic factors associated with variable and heterogeneous non-planktonic in a mutant lacking rpoN unique to CFT073 bacteria. The aim was to try to understand why RpoN suppresses this heterogeneity in the wild-type during colony growth, but also asses why this phenotype does not occur in other pathogenic strains by also sequencing transcripts from EHEC EDL933. The rpoN mutant strains was complemented with plasmid-borne rpoN containing its native promoter to ensure any differences in gene expression could solely be attributed to the absence of rpoN alone.
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