Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, rpoS gene was identified from Edwardsiella tarda EIB202 and its functional role was analyzed by using an in-frame deletion mutant rpoS and the complemental strain rpoS (+). Compared with the wild type and rpoS (+), rpoS was impaired in terms of the ability to survive under oxidative stress and nutrient starvation, as well as the resistance to 50% serum of Scophthalmus maximus in 3 h, demonstrating essential roles of RpoS in stress adaptation. The rpoS mutant also displayed markedly increased chondroitinase activity and biofilm formation. Real-time polymerase chain reaction revealed that the expression level of quorum sensing autoinducer synthetase genes luxS and edwI was increased by 3.7- and 2.5-fold in the rpoS mutant strain. Those results suggested that rpoS might be involved in the negative or positive regulation of chondroitinase and biofilm formation, or quorum sensing networks in E. tarda, respectively. Although there were no obvious differences between the wild-type and the rpoS mutant in adherence of epithelioma papulosum cyprini (EPC) cell and in the lethality on fish model, rpoS deletion leads to the drastically reduced capacity for E. tarda to internalize in EPC cells, indicating that RpoS was, while not the main, the factor required for the virulence network of E. tarda.
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PMID:Characterization of Edwardsiella tarda rpoS: effect on serum resistance, chondroitinase activity, biofilm formation, and autoinducer synthetases expression. 1928 79

To identify virulence-associated genes of a fish pathogen Yersinia ruckeri, we screened a total of 1056 mini-Tn5-Km2 signature-tagged mutants in rainbow trout by immersion challenge. Of 1056, 25 mutants were found survival-defective as they could not be re-isolated from fish kidney 7 days after infection. Mutated gene in F2-4 mutant, one of the 25 mutants, was homologous to uvrY that encodes UvrY response regulator of BarA-UvrY two-component system (TCS). Mutant F2-4 was significantly more sensitive (P < 0.05) to H2O2-mediated killing and was less able to infect Epithelioma papulosum cyprini cells. However, UvrY mutation did not affect survival of F2-4 mutant in the presence of non-immune fish serum and its ability to grow under iron starvation. In a time-course co-infection, mutant F2-4 had lower bacterial loads on day 1 itself, and by day 5 there was nearly a 1,000-fold difference in infection levels of the parent and mutant strains. The barA homolog of Y. ruckeri was PCR-amplified and sequence analyses identified four domains that were characteristic of hybrid histidine kinases. To conclude, the BarA-UvrY TCS contributes to the pathogenesis of Y. ruckeri in its natural host rainbow trout, possibly by regulating invasion of epithelial cells and sensitivity to oxidative stress induced by immune cells.
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PMID:The UvrY response regulator of the BarA-UvrY two-component system contributes to Yersinia ruckeri infection of rainbow trout (Oncorhynchus mykiss). 2048 Mar 60