Regulation of pga Operon Expression and Biofilm Formation in Actinobacillus pleuropneumoniae by σE and H-NS

ABSTRACT Clinical isolates of the porcine pathogen Actinobacillus pleuropneumoniae often form adherent colonies on agar plates due to expression of an operon, pgaABCD, encoding a poly-β-1,6-N-acetyl-d-glucosamine (PGA) extracellular matrix. The adherent colony phenotype, which correlates with the ability to form biofilms on the surfaces of polystyrene plates, is lost following serial passage in broth culture, and repeated passage of the nonadherent variants on solid media does not result in reversion to the adherent colony phenotype. In order to investigate the regulation of PGA expression and biofilm formation in A. pleuropneumoniae, we screened a bank of transposon mutants of the nonadherent serovar 1 strain S4074T and identified mutations in two genes, rseA and hns, which resulted in the formation of the adherent colony phenotype. In other bacteria, including the Enterobacteriaceae, H-NS acts as a global gene regulator, and RseA is a negative regulator of the extracytoplasmic stress response sigma factor σE. Transcription profiling of A. pleuropneumoniae rseA and hns mutants revealed that both σE and H-NS independently regulate expression of the pga operon. Transcription of the pga operon is initiated from a σE promoter site in the absence of H-NS, and upregulation of σE is sufficient to displace H-NS, allowing transcription to proceed. In A. pleuropneumoniae, H-NS does not act as a global gene regulator but rather specifically regulates biofilm formation via repression of the pga operon. Positive regulation of the pga operon by σE indicates that biofilm formation is part of the extracytoplasmic stress response in A. pleuropneumoniae.

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The co-chaperone Fkbp5 shapes the acute stress response in the paraventricular nucleus of the hypothalamus of male mice

Molecular Psychiatry ◽

10.1038/s41380-021-01044-x ◽

2021 ◽

Author(s):

Alexander S. Häusl ◽

Lea M. Brix ◽

Jakob Hartmann ◽

Max L. Pöhlmann ◽

Juan-Pablo Lopez ◽

...

Keyword(s):

Stress Response ◽

Hpa Axis ◽

Paraventricular Nucleus ◽

Acute Stress ◽

Negative Regulator ◽

Neuron Activity ◽

Cell Type ◽

Specific Expression ◽

Acute Stress Response ◽

Cell Type Specific

AbstractDisturbed activation or regulation of the stress response through the hypothalamic-pituitary-adrenal (HPA) axis is a fundamental component of multiple stress-related diseases, including psychiatric, metabolic, and immune disorders. The FK506 binding protein 51 (FKBP5) is a negative regulator of the glucocorticoid receptor (GR), the main driver of HPA axis regulation, and FKBP5 polymorphisms have been repeatedly linked to stress-related disorders in humans. However, the specific role of Fkbp5 in the paraventricular nucleus of the hypothalamus (PVN) in shaping HPA axis (re)activity remains to be elucidated. We here demonstrate that the deletion of Fkbp5 in Sim1+ neurons dampens the acute stress response and increases GR sensitivity. In contrast, Fkbp5 overexpression in the PVN results in a chronic HPA axis over-activation, and a PVN-specific rescue of Fkbp5 expression in full Fkbp5 KO mice normalizes the HPA axis phenotype. Single-cell RNA sequencing revealed the cell-type-specific expression pattern of Fkbp5 in the PVN and showed that Fkbp5 expression is specifically upregulated in Crh+ neurons after stress. Finally, Crh-specific Fkbp5 overexpression alters Crh neuron activity, but only partially recapitulates the PVN-specific Fkbp5 overexpression phenotype. Together, the data establish the central and cell-type-specific importance of Fkbp5 in the PVN in shaping HPA axis regulation and the acute stress response.

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The ClpP Protease Is Required for the Stress Tolerance and Biofilm Formation in Actinobacillus pleuropneumoniae

PLoS ONE ◽

10.1371/journal.pone.0053600 ◽

2013 ◽

Vol 8 (1) ◽

pp. e53600 ◽

Cited By ~ 32

Author(s):

Fang Xie ◽

Yanhe Zhang ◽

Gang Li ◽

Long Zhou ◽

Siguo Liu ◽

...

Keyword(s):

Stress Tolerance ◽

Biofilm Formation ◽

Actinobacillus Pleuropneumoniae

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Biofilm Formation in Pseudomonas aeruginosa: Fimbrial cup Gene Clusters Are Controlled by the Transcriptional Regulator MvaT

Journal of Bacteriology ◽

10.1128/jb.186.9.2880-2890.2004 ◽

2004 ◽

Vol 186 (9) ◽

pp. 2880-2890 ◽

Cited By ~ 102

Author(s):

Isabelle Vallet ◽

Stephen P. Diggle ◽

Rachael E. Stacey ◽

Miguel Cámara ◽

Isabelle Ventre ◽

...

Keyword(s):

Pseudomonas Aeruginosa ◽

Biofilm Formation ◽

Dna Microarrays ◽

Transcriptional Profiling ◽

Bacterial Pathogen ◽

Gene Clusters ◽

Northern Blotting ◽

Negative Regulator ◽

Regulatory Control ◽

Homologous Gene

ABSTRACT Pseudomonas aeruginosa is an opportunistic bacterial pathogen which poses a major threat to long-term-hospitalized patients and individuals with cystic fibrosis. The capacity of P. aeruginosa to form biofilms is an important requirement for chronic colonization of human tissues and for persistence in implanted medical devices. Various stages of biofilm formation by this organism are mediated by extracellular appendages, such as type IV pili and flagella. Recently, we identified three P. aeruginosa gene clusters that were termed cup (chaperone-usher pathway) based on their sequence relatedness to the chaperone-usher fimbrial assembly pathway in other bacteria. The cupA gene cluster, but not the cupB or cupC cluster, is required for biofilm formation on abiotic surfaces. In this study, we identified a gene (mvaT) encoding a negative regulator of cupA expression. Such regulatory control was confirmed by several approaches, including lacZ transcriptional fusions, Northern blotting, and transcriptional profiling using DNA microarrays. MvaT also represses the expression of the cupB and cupC genes, although the extent of the regulatory effect is not as pronounced as with cupA. Consistent with this finding, mvaT mutants exhibit enhanced biofilm formation. Although the P. aeruginosa genome contains a highly homologous gene, mvaU, the repression of cupA genes is MvaT specific. Thus, MvaT appears to be an important regulatory component within a complex network that controls biofilm formation and maturation in P. aeruginosa.

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Autoinducer-2 Triggers the Oxidative Stress Response in Mycobacterium avium, Leading to Biofilm Formation

Applied and Environmental Microbiology ◽

10.1128/aem.02066-07 ◽

2008 ◽

Vol 74 (6) ◽

pp. 1798-1804 ◽

Cited By ~ 51

Author(s):

Henriette Geier ◽

Serge Mostowy ◽

Gerard A. Cangelosi ◽

Marcel A. Behr ◽

Timothy E. Ford

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Quorum Sensing ◽

Mycobacterium Avium ◽

Biofilm Formation ◽

Transcriptional Response ◽

Opportunistic Pathogen ◽

Environmental Stresses ◽

Oxidative Stress Response ◽

Autoinducer 2

ABSTRACT Mycobacterium avium is an environmental organism and opportunistic pathogen with inherent resistance to drugs, environmental stresses, and the host immune response. To adapt to these disparate conditions, M. avium must control its transcriptional response to environmental cues. M. avium forms biofilms in various environmental settings, including drinking water pipes and potable water reservoirs. In this study, we investigated the role of the universal signaling molecule autoinducer-2 (AI-2) in biofilm formation by M. avium. The addition of the compound to planktonic M. avium cultures resulted in increased biofilm formation. Microarray and reverse transcriptase PCR studies revealed an upregulation of the oxidative stress response upon addition of AI-2. This suggests that the response to AI-2 might be related to oxidative stress, rather than quorum sensing. Consistent with this model, addition of hydrogen peroxide, a known stimulus of the oxidative stress response, to M. avium cultures resulted in elevated biofilm formation. These results suggest that AI-2 does not act as a quorum-sensing signal in M. avium. Instead, biofilm formation is triggered by environmental stresses of biotic and abiotic origins and AI-2 may exert effects on that level.

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Analysis on Actinobacillus pleuropneumoniae LuxS regulated genes reveals pleiotropic roles of LuxS/AI-2 on biofilm formation, adhesion ability and iron metabolism

Microbial Pathogenesis ◽

10.1016/j.micpath.2011.02.002 ◽

2011 ◽

Vol 50 (6) ◽

pp. 293-302 ◽

Cited By ~ 26

Author(s):

Lu Li ◽

Zhuofei Xu ◽

Yang Zhou ◽

Tingting Li ◽

Lili Sun ◽

...

Keyword(s):

Iron Metabolism ◽

Biofilm Formation ◽

Actinobacillus Pleuropneumoniae ◽

Adhesion Ability

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Make and break the alarmone: regulation of (p)ppGpp synthetase/hydrolase enzymes in bacteria

FEMS Microbiology Reviews ◽

10.1093/femsre/fuz009 ◽

2019 ◽

Vol 43 (4) ◽

pp. 389-400 ◽

Cited By ~ 37

Author(s):

Séverin Ronneau ◽

Régis Hallez

Keyword(s):

Cell Cycle ◽

Stress Response ◽

Stress Responses ◽

Biofilm Formation ◽

Pathogenic Bacteria ◽

Second Messengers ◽

Molecular Devices ◽

Environmental Cues ◽

Fluctuating Environments ◽

Harsh Conditions

ABSTRACTBacteria use dedicated mechanisms to respond adequately to fluctuating environments and to optimize their chances of survival in harsh conditions. One of the major stress responses used by virtually all bacteria relies on the sharp accumulation of an alarmone, the guanosine penta- or tetra-phosphate commonly referred to as (p)ppGpp. Under stressful conditions, essentially nutrient starvation, these second messengers completely reshape the metabolism and physiology by coordinately modulating growth, transcription, translation and cell cycle. As a central regulator of bacterial stress response, the alarmone is also involved in biofilm formation, virulence, antibiotics tolerance and resistance in many pathogenic bacteria. Intracellular concentrations of (p)ppGpp are determined by a highly conserved and widely distributed family of proteins called RelA-SpoT Homologs (RSH). Recently, several studies uncovering mechanisms that regulate RSH activities have renewed a strong interest in this field. In this review, we outline the diversity of the RSH protein family as well as the molecular devices used by bacteria to integrate and transform environmental cues into intracellular (p)ppGpp levels.

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FK506-binding protein FklB is involved in biofilm formation through its peptidyl-prolyl isomerase activity

10.1101/2020.02.01.930347 ◽

2020 ◽

Author(s):

Chrysoula Zografou ◽

Maria Dimou ◽

Panagiotis Katinakis

Keyword(s):

Biofilm Formation ◽

Negative Regulator ◽

Cell Length ◽

Wild Type ◽

Prolyl Isomerase ◽

Ppiase Activity ◽

Peptidyl Prolyl Isomerase ◽

Knock Out ◽

E Coli ◽

The Mean

AbstractFklB is a member of the FK506-binding proteins (FKBPs), a family that consists of five genes in Escherichia coli. Little is known about the physiological and functional role of FklB in bacterial movement. In the present study, FklB knock-out mutant ΔfklB presented an increased swarming and swimming motility and biofilm formation phenotype, suggesting that FklB is a negative regulator of these cellular processes. Complementation with Peptidyl-prolyl isomerase (PPIase)-deficient fklB gene (Y181A) revealed that the defects in biofilm formation were not restored by Y181A, indicating that PPIase activity of FklB is modulating biofilm formation in E. coli. The mean cell length of ΔfklB swarming cells was significantly smaller as compared to the wild-type BW25113. Furthermore, the mean cell length of swarming and swimming wild-type and ΔfklB cells overexpressing fklB or Y181A was considerably larger, suggesting that PPIase activity of FklB plays a role in cell elongation and/or cell division. A multi-copy suppression assay demonstrated that defects in motility and biofilm phenotype were compensated by overexpressing sets of PPIase-encoding genes. Taken together, our data represent the first report demonstrating the involvement of FklB in cellular functions of E. coli.

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Constitutive Photomorphogenic 1 Enhances ER Stress Tolerance in Arabidopsis

International Journal of Molecular Sciences ◽

10.3390/ijms221910772 ◽

2021 ◽

Vol 22 (19) ◽

pp. 10772

Author(s):

Chang Ho Kang ◽

Eun Seon Lee ◽

Ganesh M. Nawkar ◽

Joung Hun Park ◽

Seong Dong Wi ◽

...

Keyword(s):

Stress Response ◽

Er Stress ◽

Stress Conditions ◽

Negative Regulator ◽

Light Signaling ◽

Dependent Manner ◽

Wild Type ◽

Er Stress Response ◽

The Unfolded Protein Response ◽

Mutant Locus

Interaction between light signaling and stress response has been recently reported in plants. Here, we investigated the role of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), a key regulator of light signaling, in endoplasmic reticulum (ER) stress response in Arabidopsis. The cop1-4 mutant Arabidopsis plants were highly sensitive to ER stress induced by treatment with tunicarmycin (Tm). Interestingly, the abundance of nuclear-localized COP1 increased under ER stress conditions. Complementation of cop1-4 mutant plants with the wild-type or variant types of COP1 revealed that the nuclear localization and dimerization of COP1 are essential for its function in plant ER stress response. Moreover, the protein amount of ELONGATED HYPOCOTYL 5 (HY5), which inhibits bZIP28 to activate the unfolded protein response (UPR), decreased under ER stress conditions in a COP1-dependent manner. Accordingly, the binding of bZIP28 to the BIP3 promoter was reduced in cop1-4 plants and increased in hy5 plants compared with the wild type. Furthermore, introduction of the hy5 mutant locus into the cop1-4 mutant background rescued its ER stress-sensitive phenotype. Altogether, our results suggest that COP1, a negative regulator of light signaling, positively controls ER stress response by partially degrading HY5 in the nucleus.

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