Yersinia pseudotuberculosis
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ABSTRACT:
PROVIDER: PRJNA237009 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The pyruvate-tricarboxylic acid cycle node: a focal point of virulence control in the enteric pathogen Yersinia pseudotuberculosis [crp mutant]
| PRJNA237011 | ENA
Project description:The pyruvate-tricarboxylic acid cycle node: a focal point of virulence control in the enteric pathogen Yersinia pseudotuberculosis [rovA mutant]
| PRJNA237010 | ENA
Project description:Whole transcriptome assessment of the Yersinia pseudotuberculosis strain YPIII. The Y. pseudotuberculosis csrA regulon was determined in Yersinia minimal minimum developed for the study. CsrA is a key regulator coordinating virulence and metabolism.
2014-09-17 | GSE54545 | GEO
Project description:Whole transcriptome assessment of the Yersinia pseudotuberculosis strain YPIII. The Y. pseudotuberculosis csrA regulon was determined in Yersinia minimal minimum developed for the study. CsrA is a key regulator coordinating virulence and metabolism. Y. pseudotuberculosis YPIII or the isogenic csrA mutant strain were cultivated at 25M-BM-0C under aeration on a rotary shaker. First pre-cultures were grown in a 1:1 mixture of HAMM-bM-^@M-^Ys F-12 Nutrient Mixture (Invitrogen, Carlsbad, US) and liquid DMEM medium (Biochrom, Berlin, DE). Second pre-cultures and main cultures were grown in a Yersinia minimal medium (YMM). The analysis comprised three biological replicates for each strain. In addition, samples, taken at three different time points of the exponential growth phase, were used to validate constant expression during the cultivation. Total RNA was extracted using SV Total RNA Isolation System (Promega). The samples were treated with RNase-free DNase (Roche Applied Science) and the quality of the RNA was confirmed by the lack of PCR amplification of the hns gene and by using an Agilent 2100 Bioanalyzer.
2014-09-17 | E-GEOD-54545 | biostudies-arrayexpress
Project description:Whole transcriptome assessment of the Yersinia pseudotuberculosis strain YPIII. The Y. pseudotuberculosis rovA regulon was determined in Yersinia minimal minimum developed for the study. RovA is a key regulator for Yersinia virulence.
2014-09-17 | GSE54546 | GEO
Project description:Whole transcriptome assessment of the Yersinia pseudotuberculosis strain YPIII. The Y. pseudotuberculosis crp regulon was determined in Yersinia minimal minimum developed for the study. Crp is a key regulator coordinating virulence and metabolism.
2014-09-17 | GSE54544 | GEO
Project description:Expression of the virulence regulator RovA of Yersinia pseudotuberculosis, is controlled by the ncRNAs CsrB and CsrC through CsrA and RovM. In this study, we show that the regulator YmoA of the Hha family of nucleoid-associated proteins controls expression of the counterregulated Csr-type RNAs and the Csr-RovM-RovA signalling cascade through alterations of the CsrC RNA stability. YmoA-mediated stabilization of CsrC depends on CsrA and H-NS, but not on the RNA chaperone Hfq and involves a stabilizing stem-loop structure within the 5M-bM-^@M-^Y-region of CsrC. YmoA influence on CsrC stability is complex as YmoA was found to control numerous factors known to affect RNA structures and stability. In addition, YmoA controls temperature-dependent early and later stage virulence genes in an opposite manner and coregulates their expression with bacterial stress responses and metabolic functions. Following oral infections in a mouse model, we demonstrate that a ymoA mutant is strongly reduced in its ability to disseminate to the PeyerM-bM-^@M-^Ys patches, mesenteric lymph nodes, liver and spleen and exhibits a reduced mortality. We propose a model in which YmoA controls switching from a RovA-dependent early colonization phase towards a virulence plasmid (pYV)-dependent infection phase important for host defense and persistence. For each microarray, 300ng of each Cy3- and Cy5-labelled RNA were mixed, fragmented and hybridized to the microarray at 65M-BM-0C for 17 hours using the Agilent Hybridization Chamber according to the Agilent instructions. Four replicates were performed. Sequences used for the design of the microarray (Agilent, 8 x 15K format) include three different 60-nt oligonucleotides for all 4172 chromosomal genes (ORFs > 30 codons) of the Y. pseudotuberculosis YPIII genome and six probes for the 92 genes of the virulence plasmid pYV of Y. pseudotuberculosis strain IP32953.
2012-07-30 | E-GEOD-35043 | biostudies-arrayexpress
Project description:Yersinia pestis, the etiologic agent of plague, emerged as a flea-borne pathogen only within the last 6,000 years. Just five simple genetic changes in the Yersinia pseudotuberculosis progenitor, which served to eliminate toxicity to fleas and to enhance survival and biofilm formation in the flea digestive tract, were key to the transition to the arthropod-borne transmission route. To gain a deeper understanding of the genetic basis for the development of a transmissible biofilm infection in the flea foregut, we evaluated additional gene differences and performed in vivo transcriptional profiling of Y. pestis, Y. pseudotuberculosis wild-type (unable to form biofilm in the flea foregut), and a Y. pseudotuberculosis mutant strain (able to produce foregut-blocking biofilm in fleas) recovered from fleas 1 day and 14 days after an infectious bloodmeal. Surprisingly, the Y. pseudotuberculosis mutations that increased c-di-GMP levels and enabled biofilm development in the flea did not change expression levels of the hms genes responsible for the synthesis and export of the extracellular polysaccharide matrix required for mature biofilm formation. The Y. pseudotuberculosis mutant uniquely expressed much higher levels of one of the Yersinia Type VI secretion systems (T6SS-4) in the flea, and this locus was required for flea blockage by Y. pseudotuberculosis, but not by Y. pestis. Significant differences between the two species in expression of several metabolism genes, the Psa fimbrial genes, quorum sensing related genes, transcriptional regulators, and stress response genes were evident during flea infection. The results provide insights into how Y. pestis has adapted to life in its flea vector and point to evolutionary changes in the regulation of biofilm development pathways in these two closely related species
2019-01-28 | GSE119243 | GEO
Project description:Expression of the virulence regulator RovA of Yersinia pseudotuberculosis, is controlled by the ncRNAs CsrB and CsrC through CsrA and RovM. In this study, we show that the regulator YmoA of the Hha family of nucleoid-associated proteins controls expression of the counterregulated Csr-type RNAs and the Csr-RovM-RovA signalling cascade through alterations of the CsrC RNA stability. YmoA-mediated stabilization of CsrC depends on CsrA and H-NS, but not on the RNA chaperone Hfq and involves a stabilizing stem-loop structure within the 5’-region of CsrC. YmoA influence on CsrC stability is complex as YmoA was found to control numerous factors known to affect RNA structures and stability. In addition, YmoA controls temperature-dependent early and later stage virulence genes in an opposite manner and coregulates their expression with bacterial stress responses and metabolic functions. Following oral infections in a mouse model, we demonstrate that a ymoA mutant is strongly reduced in its ability to disseminate to the Peyer’s patches, mesenteric lymph nodes, liver and spleen and exhibits a reduced mortality. We propose a model in which YmoA controls switching from a RovA-dependent early colonization phase towards a virulence plasmid (pYV)-dependent infection phase important for host defense and persistence.
2012-07-31 | GSE35043 | GEO