Phenotypic and transcriptional analysis of the osmotic regulator OmpR in Yersinia pestis

Gao, He; Zhang, Yiquan; Han, Yanping; Yang, Lin; Liu, Xia; Guo, Zhaobiao; Tan, Yafang; Huang, Xinxiang; Zhou, Dongsheng; Yang, Ruifu

doi:10.1186/1471-2180-11-39

Cited by 48 publications

(55 citation statements)

References 43 publications

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“…Hence, Y. pseudotuberculosis and Y. pestis may have several suppressor mutations, i.e., a very different regulatory network compared with the above-mentioned bacteria. Consistently, Y. pestis has altered Rcs and cyclic di-GMP signaling pathways and does not control ompF and ompC (involved in bacterial adaptation to osmotic conditions) in the same way as E. coli and D. dadantii (13,62,63). However, whatever applies to Y. pestis might not apply to Y. pseudotuberculosis, since the latter has a functional Rcs system and does not control its c-di-GMP signaling pathways in the same way as the former.…”

Section: Discussionmentioning

confidence: 83%

Evaluation of the Role of the opgGH Operon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestis

et al. 2015

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fThe opgGH operon encodes glucosyltransferases that synthesize osmoregulated periplasmic glucans (OPGs) from UDP-glucose, using acyl carrier protein (ACP) as a cofactor. OPGs are required for motility, biofilm formation, and virulence in various bacteria. OpgH also sequesters FtsZ in order to regulate cell size according to nutrient availability. Yersinia pestis (the agent of fleaborne plague) lost the opgGH operon during its emergence from the enteropathogen Yersinia pseudotuberculosis. When expressed in OPG-negative strains of Escherichia coli and Dickeya dadantii, opgGH from Y. pseudotuberculosis restored OPGs synthesis, motility, and virulence. However, Y. pseudotuberculosis did not produce OPGs (i) under various growth conditions or (ii) when overexpressing its opgGH operon, its galUF operon (governing UDP-glucose), or the opgGH operon or Acp from E. coli. A ⌬opgGH Y. pseudotuberculosis strain showed normal motility, biofilm formation, resistance to polymyxin and macrophages, and virulence but was smaller. Consistently, Y. pestis was smaller than Y. pseudotuberculosis when cultured at >37°C, except when the plague bacillus expressed opgGH. Y. pestis expressing opgGH grew normally in serum and within macrophages and was fully virulent in mice, suggesting that small cell size was not advantageous in the mammalian host. Lastly, Y. pestis expressing opgGH was able to infect Xenopsylla cheopis fleas normally. Our results suggest an evolutionary scenario whereby an ancestral Yersinia strain lost a factor required for OPG biosynthesis but kept opgGH (to regulate cell size). The opgGH operon was presumably then lost because OpgH-dependent cell size control became unnecessary. Yersinia pestis is the bacterium that causes plague, a fatal disease that cycles between mammalian and flea hosts (1). After Y. pestis is taken up into a flea's gut during a blood meal, the bacterium forms a biofilm that ultimately obstructs the digestive tract. The "blocked" (and thus starving) flea will bite a new host many times in an effort to feed. During these unproductive attempts to feed, some bacteria are dislodged from the biofilm and regurgitated into the dermal biting site (2-4). Although it is not clear whether these Y. pestis organisms are truly phagocytized, it generally assumed that they replicate initially within phagocytes and produce antiphagocytic factors; this leads to extracellular replication throughout the draining lymph node and ultimately in the blood and other deep tissues (5).Y. pestis emerged from Yersinia pseudotuberculosis, a widely spread environmental bacterium that causes a mild bowel disease in humans following ingestion of contaminated foods (6). During its emergence, Y. pestis accreted a small amount of genetic material via horizontal transfer but also lost a large number of functional genes (7). Early investigations showed that the emergence of plague can be explained (at least in part) by the acquisition of genetic material (8-11). Hence, a stepwise scenario in which sequential gene losses led to a flea-b...

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Section: Discussionmentioning

confidence: 83%

Evaluation of the Role of the opgGH Operon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestis

et al. 2015

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“…Deletion of OmpR in Y. pestis CO92 resulted in differential expression of 224 genes, including repression of cas1 transcription ( Fig. 1 and 4) (73). The cas1 gene was also slightly downregulated during the preadaptation phase, when the Y. pestis CO92 strain adapted itself to the environment in fleas that parasitize rats ( Fig.…”

Section: Transcriptome Analysis Of the Cas Genesmentioning

confidence: 99%

“…1 and 4), among other gene transcripts (73). It is noteworthy that Y. pestis OmpR and Cas1 are involved in the stress response (73), which is reminiscent of the involvement of transcriptional regulators and the CRISPR-Cas systems in the stress responses of E. coli and M. xanthus.…”

Section: Transcriptome Analysis Of the Cas Genesmentioning

confidence: 99%

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The Role of CRISPR-Cas Systems in Virulence of Pathogenic Bacteria

Louwen

Staals

Endtz

et al. 2014

Microbiol Mol Biol Rev

219

178

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SUMMARY Clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated (Cas) genes are present in many bacterial and archaeal genomes. Since the discovery of the typical CRISPR loci in the 1980s, well before their physiological role was revealed, their variable sequences have been used as a complementary typing tool in diagnostic, epidemiologic, and evolutionary analyses of prokaryotic strains. The discovery that CRISPR spacers are often identical to sequence fragments of mobile genetic elements was a major breakthrough that eventually led to the elucidation of CRISPR-Cas as an adaptive immunity system. Key elements of this unique prokaryotic defense system are small CRISPR RNAs that guide nucleases to complementary target nucleic acids of invading viruses and plasmids, generally followed by the degradation of the invader. In addition, several recent studies have pointed at direct links of CRISPR-Cas to regulation of a range of stress-related phenomena. An interesting example concerns a pathogenic bacterium that possesses a CRISPR-associated ribonucleoprotein complex that may play a dual role in defense and/or virulence. In this review, we describe recently reported cases of potential involvement of CRISPR-Cas systems in bacterial stress responses in general and bacterial virulence in particular.

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“…Bacteria typically counteract such fluctuations through the compensatory accumulation or expulsion of compatible solutes that restore osmotic balance in the cells. In addition, pathogenic bacteria have virulenceassociated osmosensory mechanisms that are triggered at the transcriptional level [13,14]. It can be conclude that increasing sodium chloride concentration could decrease viability of cells and cell division patterns.…”

Section: Discussionmentioning

confidence: 99%

Effect of Environmental Stresses on Growth Pattern, Biofilm Formation and Biochemical Characteristics of Mycobacterium marinum CCUG20998

Ghasemi

Moslem

Mirpour

2016

Zahedan J Res Med Sci

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Background: Mycobacterium marinum is a ubiquitous, slow-growing nontuberclosis Mycobacterium (NTM), it can causes disseminated granulomatous infections in fish. Outbreaks in fisheries can be financially devastating and can also increase the chance of human exposure. Objectives: The aim of this work was evaluating the effects of some environmental stresses on M. marinum CCUG 20998. Methods: In this descriptive-analytic study M. marinum CCUG 20998 was subjected to different conditions of environmental stresses such as pH, oxidative, osmotic pressure, and temperatures. The effects of stresses were studied on growth, biofilm formation, and cell division and biochemical characteristics of M. marinum CCUG 20998.The growth data were analyzed by measuring colony forming unit (CFU) using SPSS software version 19. Results:The results showed that sodium chloride and hydrogen peroxide at %10 and 9600 ppm concentrations inhibit. Marinum CCUG 20998 growths, respectively. Tolerance to pH = 11 and temperature at 82.5°C was detectable. Also, environmental stresses could affects on some biochemical characteristics of M. marinum CCUG 20998. Biofilm formation reduced upon using all stress conditions. Conclusions: Bacteria are able to adapt to dramatically different environments, In the case of mycobacteria, there is direct correlation between stress and pathogenicity. The results obtained from this study provided useful information on survival and tolerance of M. marinum CCUG 20998 to different environmental conditions. Survival under stress conditions might not reflect the in vivo situation where host factors also contribute to establishment of the organism during infection.

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Phenotypic and transcriptional analysis of the osmotic regulator OmpR in Yersinia pestis

Cited by 48 publications

References 43 publications

Evaluation of the Role of the opgGH Operon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestis

Evaluation of the Role of the opgGH Operon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestis

The Role of CRISPR-Cas Systems in Virulence of Pathogenic Bacteria

Effect of Environmental Stresses on Growth Pattern, Biofilm Formation and Biochemical Characteristics of Mycobacterium marinum CCUG20998

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