scholarly journals Role of the FliA-FlgM regulatory system on the transcriptional control of the flagellar regulon and flagellar formation in Salmonella typhimurium.

1994 ◽  
Vol 176 (12) ◽  
pp. 3598-3605 ◽  
Author(s):  
K Kutsukake ◽  
T Iino
Keyword(s):  
Salmonella Typhimurium ◽  
Transcriptional Control ◽  
Regulatory System ◽  
Flagellar Regulon

scholarly journals Magnesium and the Role of mgtC in Growth of Salmonella typhimurium

1998 ◽  
Vol 66 (8) ◽  
pp. 3802-3809 ◽  
Author(s):  
Mary Beth C. Moncrief ◽  
Michael E. Maguire
Keyword(s):  
Salmonella Typhimurium ◽  
Minimal Medium ◽  
Regulatory System ◽  
Low Ph ◽  
Transport Systems ◽  
Lag Phase ◽  
Primary Role ◽  
Cation Uptake ◽  
P Type

ABSTRACT Salmonella typhimurium has three distinct transport systems for Mg2+: CorA, MgtA, and MgtB. ThemgtCB operon encodes two proteins, MgtC, a hydrophobic protein with a predicted molecular mass of 22.5 kDa, and MgtB, a 102-kDa P-type ATPase Mg2+ transport protein. ThemgtCB locus has been identified as part of a newSalmonella pathogenicity island, SPI-3. Transcription ofmgtCB is regulated by extracellular Mg2+ via the two-component PhoPQ regulatory system important for virulence. To elucidate MgtC’s role in a low-Mg2+ environment, we looked at growth and transport in strains lacking the CorA and MgtA Mg2+ transporters but expressing MgtB, MgtC, or both.mgtC mgtB+ and mgtC+mgtB+ strains exhibited growth in N minimal medium without added Mg2+ with a 1- to 2-h lag phase. AnmgtC+ mgtB strain was also able to grow in N minimal medium without added Mg2+ but only after a 24-h lag phase. In N minimal medium containing 10 mM Mg2+, all strains grew after a short lag phase; the mgtC+mgtB strain grew to a higher optical density at 600 nm than anmgtC+ mgtB+ strain and was comparable to wild type. The lengthy lag phase before growth in anmgtC+ mgtB strain was not due to lack of expression of MgtC. Western blot analysis indicated that substantial MgtC protein is present by 2 h after suspension in N minimal medium. Surprisingly, in an mgtC+mgtB+ strain, MgtC was undetectable during Mg2+ starvation, although large amounts of MgtB were observed. The lack of expression of MgtC is not dependent on functional MgtB, since a strain carrying a nonfunctional MgtB with a mutation (D379A) also did not make MgtC. Since, during invasion of eukaryotic cells, S. typhimurium appears to be exposed to a low-pH as well as a low-Mg2+ environment, the growth of anmgtC+ mgtB strain was tested at low pH with and without added Mg2+. While significant quantities of MgtC could be detected after suspension at pH 5.2, themgtC+ mgtB strain was unable to grow at pH 5.2 whether or not Mg2+ was present. Finally, using63Ni2+ and 57Co2+ as alternative substrates for the unavailable28Mg2+, cation uptake could not be detected in an mgtC+ mgtB strain after Mg2+starvation. We conclude that MgtC is not a Mg2+ transporter and that it does not have a primary role in the survival of S. typhimurium at low pH.

scholarly journals Redefining the Role of the β-Lactamase Locus in Methicillin-Resistant Staphylococcus aureus: β-Lactamase Regulators Disrupt the MecI-Mediated Strong Repression onmecAand Optimize the Phenotypic Expression of Resistance in Strains with ConstitutivemecAExpression

2013 ◽  
Vol 57 (7) ◽  
pp. 3037-3045 ◽  
Author(s):  
Pedro Arêde ◽  
Joana Ministro ◽  
Duarte C. Oliveira
Keyword(s):  
Staphylococcus Aureus ◽  
Transcriptional Control ◽  
Phenotypic Expression ◽  
Regulatory System ◽  
Methicillin Resistant ◽  
Content Type ◽  
Resistance Determinants ◽  
Regulatory Systems ◽  
Mrsa Strains

ABSTRACTIn response to β-lactam chemotherapy,Staphylococcus aureushas acquired two resistance determinants:blaZ, coding for β-lactamase, which confers resistance to penicillins only, andmecA, coding for an extra cell wall cross-linking enzyme with reduced affinity for virtually all other β-lactams. The transcriptional control of both resistance determinants is regulated by homologous repressors (BlaI and MecI, respectively) and sensor inducers (BlaR1 and MecR1, respectively). There is a cross-talk between the two regulatory systems, and it has been demonstrated thatblaregulators stabilize themecAacquisition. In a recent study, we have unexpectedly observed that in most MRSA strains, there was no significant change in the resistance phenotype upon the overexpression intransof a MecI repressor, whereas in those few strains negative for theblalocus, there was a massive decrease of resistance (D. C. Oliveira and H. de Lencastre, PLoS One 6:e23287, 2011). Here, we demonstrate that, contrary to what is currently accepted, theblaregulatory system efficiently disrupts the strong MecI-mediated repression onmecA, enabling the optimal expression of resistance. This effect appears to be due to the formation of MecI::BlaI heterodimers that might bind less efficiently to themecApromoter and become nonfunctional due to the proteolytic inactivation of the BlaI monomer. In addition, we have also observed that the presence ofblaregulators may enhance dramatically the expression of β-lactam resistance in MRSA strains with constitutivemecAexpression, compensating for the fitness cost imposed by the large β-lactamase plasmid. These observations point to important unrecognized roles of theblalocus for the expression of the methicillin-resistantS. aureus(MRSA) phenotype.

THYROID STIMULATORS AND THYROID STIMULATION

1971 ◽  
Vol 66 (3) ◽  
pp. 558-576 ◽  
Author(s):  
Gerald Burke
Keyword(s):  
Regulatory System ◽  
Control Site ◽  
Thyroid Cell ◽  
Primary Control ◽  
Physico Chemical ◽  
Site Of Action ◽  
Long Acting

ABSTRACT A long-acting thyroid stimulator (LATS), distinct from pituitary thyrotrophin (TSH), is found in the serum of some patients with Graves' disease. Despite the marked physico-chemical and immunologic differences between the two stimulators, both in vivo and in vitro studies indicate that LATS and TSH act on the same thyroidal site(s) and that such stimulation does not require penetration of the thyroid cell. Although resorption of colloid and secretion of thyroid hormone are early responses to both TSH and LATS, available evidence reveals no basic metabolic pathway which must be activated by these hormones in order for iodination reactions to occur. Cyclic 3′, 5′-AMP appears to mediate TSH and LATS effects on iodination reactions but the role of this compound in activating thyroidal intermediary metabolism is less clear. Based on the evidence reviewed herein, it is suggested that the primary site of action of thyroid stimulators is at the cell membrane and that beyond the(se) primary control site(s), there exists a multifaceted regulatory system for thyroid hormonogenesis and cell growth.

The role of a stress-response protein in Salmonella typhimurium virulence

1991 ◽  
Vol 5 (2) ◽  
pp. 401-407 ◽  
Author(s):  
K. Johnson ◽  
I. Charles ◽  
G. Dougan ◽  
D. Pickard ◽  
P. O'Gaora ◽  
...  
Keyword(s):  
Stress Response ◽  
Salmonella Typhimurium

scholarly journals Spontaneous Gac Mutants of Pseudomonas Biological Control Strains: Cheaters or Mutualists?

2011 ◽  
Vol 77 (20) ◽  
pp. 7227-7235 ◽  
Author(s):  
William W. Driscoll ◽  
John W. Pepper ◽  
Leland S. Pierson ◽  
Elizabeth A. Pierson
Keyword(s):  
Alternative Hypothesis ◽  
Natural Populations ◽  
Regulatory System ◽  
Wild Type ◽  
Content Type ◽  
The Public ◽  
Extracellular Metabolites ◽  
Mutualistic Interaction ◽  
Alternative Hypotheses

ABSTRACTBacteria rely on a range of extracellular metabolites to suppress competitors, gain access to resources, and exploit plant or animal hosts. The GacS/GacA two-component regulatory system positively controls the expression of many of these beneficial external products in pseudomonad bacteria. Natural populations often contain variants with defective Gac systems that do not produce most external products. These mutants benefit from a decreased metabolic load but do not appear to displace the wild type in nature. How could natural selection maintain the wild type in the presence of a mutant with enhanced growth? One hypothesis is that Gac mutants are “cheaters” that do not contribute to the public good, favored within groups but selected against between groups, as groups containing more mutants lose access to ecologically important external products. An alternative hypothesis is that Gac mutants have a mutualistic interaction with the wild type, so that each variant benefits by the presence of the other. In the biocontrol bacteriumPseudomonas chlororaphisstrain 30-84, Gac mutants do not produce phenazines, which suppress competitor growth and are critical for biofilm formation. Here, we test the predictions of these alternative hypotheses by quantifying interactions between the wild type and the phenazine- and biofilm-deficient Gac mutant within growing biofilms. We find evidence that the wild type and Gac mutants interact mutualistically in the biofilm context, whereas a phenazine-defective structural mutant does not. Our results suggest that the persistence of alternative Gac phenotypes may be due to the stabilizing role of local mutualistic interactions.

scholarly journals Estrogen-related receptor alpha (ERRα) is a key regulator of intestinal homeostasis and protects against colitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Allan Tran ◽  
Charlotte Scholtes ◽  
Mario Songane ◽  
Claudia Champagne ◽  
Luc Galarneau ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Current Knowledge ◽  
Experimental Colitis ◽  
Protective Effects ◽  
Mitochondrial Energy Metabolism ◽  
Receptor Alpha ◽  
Cell Counts ◽  
Α Diversity ◽  
Estrogen Related Receptor

AbstractThe estrogen-related receptor alpha (ERRα) is a primary regulator of mitochondrial energy metabolism, function and dynamics, and has been implicated in autophagy and immune regulation. ERRα is abundantly expressed in the intestine and in cells of the immune system. However, its role in inflammatory bowel disease (IBD) remains unknown. Here, we report a protective role of ERRα in the intestine. We found that mice deficient in ERRα were susceptible to experimental colitis, exhibiting increased colon inflammation and tissue damage. This phenotype was mediated by impaired compensatory proliferation of intestinal epithelial cells (IEC) following injury, enhanced IEC apoptosis and necrosis and reduced mucus-producing goblet cell counts. Longitudinal analysis of the microbiota demonstrated that loss of ERRα lead to a reduction in microbiome α-diversity and depletion of healthy gut bacterial constituents. Mechanistically, ERRα mediated its protective effects by acting within the radio-resistant compartment of the intestine. It promoted disease tolerance through transcriptional control of key genes involved in intestinal tissue homeostasis and repair. These findings provide new insights on the role of ERRα in the gut and extends our current knowledge of nuclear receptors implicated in IBD.

sRNA STnc150 is involved in virulence regulation of Salmonella Typhimurium by targeting fimA mRNA

2021 ◽  
Vol 368 (18) ◽  
Author(s):  
Jing Li ◽  
Na Li ◽  
Chengcheng Ning ◽  
Yun Guo ◽  
Chunhui Ji ◽  
...  
Keyword(s):  
Salmonella Typhimurium ◽  
Target Genes ◽  
Reporter System ◽  
Stem Loop ◽  
Viral Loads ◽  
Virulence Regulation ◽  
Stem Loop Structure ◽  
Complementary Strain

ABSTRACT Small RNAs (sRNAs) are essential virulent regulators in Salmonella typhimurium (STM). To explore the role of sRNA STnc150 in regulating STM virulence, we constructed a STnc150 deletion strain (ΔSTnc150) and its complementary strain (ΔSTnc150/C). Then, we compared their characteristics to their original parent strain experimentally, identified the target genes of STnc150 and determined the expression levels of target genes. The results showed that the ΔSTnc150 strain exhibited delayed biofilm formation, enhanced adhesion to macrophages, significantly reduced LD50, increased liver and spleen viral loads and more vital pathological damaging ability than its parent and complementary strains. Further, bioinformatics combined with the bacterial dual plasmid reporter system confirmed that the bases 72–88 of STnc150 locating at the secondary stem-loop structure of the STnc150 are complementary with the bases 1–19 in the 5′-terminal of fimA mRNA of the type 1 fimbriae subunit. Western blot analysis showed that fimA protein level was increased in STnc150 strain compared with its parent and complementary strains. Together, this study suggested that STnc150 can down-regulate STM fimA expression at the translation level, which provided insights into the regulatory mechanisms of sRNAs in virulence of STM.

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