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Yersinia pseudotuberculosis strain:6904

ABSTRACT: Yersinia pseudotuberculosis strain:6904 Genome sequencing

PROVIDER: PRJNA243514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR2180212_1.fastq.gz	Fastqsanger.gz
	SRR2180212_2.fastq.gz	Fastqsanger.gz
	SRR2180213.fastq.gz	Fastqsanger.gz

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The pyruvate-tricarboxylic acid cycle node: a focal point of virulence control in the enteric pathogen Yersinia pseudotuberculosis [rovA mutant]

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. Y. pseudotuberculosis YPIII or the isogenic rovA 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.

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Project description:We previously suggested that increased expression of the gene encoding transcriptional antiterminator RfaH during Yersinia pseudotuberculosis transcriptional reprogramming is necessary for adapting to persistent infection. In this study, we examined the role of RfaH in virulence and bacterial physiology under infection-relevant stress conditions, and identified genes differentially regulated in the absence of RfaH in Y. pseudotuberculosis. We employed a mouse infection model and phenotypic assays to test RfaH's role in virulence and physiology, as well as RNA sequencing, including O-antigen biosynthesis-deficient strains. Our findings demonstrate that loss of RfaH significantly attenuates virulence, reducing the capacity of Y. pseudotuberculosis to establish persistent infection. RfaH expression is increased during the stationary growth phase and under various stress conditions, such as high osmolarity and bile salts, which are known to induce envelope stress. Functional assays revealed that the ΔrfaH strain displayed defects in motility and increased clumping, indicating altered surface properties affecting motility. Moreover, transcriptomic profiling of the ΔrfaH strain revealed a specific RfaH-dependent gene set after filtering out genes affected by O-antigen-related mutations, thereby minimizing confounding effects from surface structure alterations. These results suggest that RfaH influences a broader set of virulence and adaptation pathways beyond O-antigen regulation. Collectively, our findings suggest that RfaH is essential for the virulence and adaptive capacity of Y. pseudotuberculosis to colonize the host. This study provides insights into regulatory mechanisms that facilitate bacterial survival in hostile environments and highlights the importance of RfaH and its regulatory targets in the pathogenesis of Y. pseudotuberculosis.

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