Transcription profiling of Arabidopsis plants over overexpressing BhHsf1
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
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PROVIDER: E-MTAB-106 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Understanding how pathogens respond to antimicrobial peptides, and how this compares to currently available antibiotics, is crucial to optimizing antibiotic therapy. Staphylococcus aureus has several known resistance mechanisms against human cationic antimicrobial peptides (CAMPs). We aim to determine how S. aureus responds to sheep and frog CAMPs, and whether this response is associated with resistance. Gene expression changes in Staphylococcus aureus Newman cells exposed to linear CAMPs were analyzed by DNA microarray. Three antimicrobial peptides were used in the analysis, two of them are derived from frog, temporin L and dermaseptin K4-S4(1-16), one is from sheep, ovispirin-1. The peptides induced the VraSR cell-wall regulon and several other genes which are also upregulated in cells treated with vancomycin and other cell wall-active antibiotics. In addition to this similarity, three genes/operons were particularly strongly induced by the peptides: vraDE, SA0205 and SAS016, encoding an ABC transporter, a putative membrane-bound lysostaphin-like peptidase and a small functionally unknown protein, respectively. Ovispirin-1 and dermaseptin K4-S4(1-16), which disrupt lipid bilayers by the carpet mechanism, were strong inducers of the vraDE operon. We show that high level induction by ovispirin-1 was dependent on the amide modification of the peptide C-terminus. This suggests that the amide group has a crucial role in the activation of the Aps sensory system, the regulator of vraDE. In contrast, temporin L, which disrupts lipid bilayers by forming pores, was clearly a weaker inducer of vraDE despite the C-terminal amide modification. Sensitivity testing with CAMPs and other antimicrobials suggested that VraDE is a transporter dedicated to resist bacitracin. We also showed that SA0205 belongs to the VraSR regulon. Furthermore, VraSR was shown to be important for resistance against a wide range of cell wall-active antibiotics and other antimicrobial agents including the amide-modified ovispirin-1, bacitracin, teicoplanin, cefotaxime and 10 other β-lactam antibiotics, chlorpromazine, thioridazine and EGTA. The effects of the three different antimicrobial peptides on gene expression of S. aureus Newman were studied by using whole genome oligo-DNA microarrays. Bacteria were grown in BHI medium to the early exponential phase (OD600=0.6) and antimicrobial peptides were added at sublethal concentrations. Samples were taken for RNA isolations after treating the cultures with the peptides for 10 minutes. Control cultures without peptide additions were treated similarly and in parallel.
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2015-12-24 | E-GEOD-42536 | biostudies-arrayexpress
Project description:Background: S. aureus is one of the main pathogen involved in ruminant mastitis worldwide. The severity of staphylococcal infection is highly variable and ranges from subclinical to gangrenous mastitis. Such variability implies host as well as staphylococcal factors. This work is an in-depth characterization of S. aureus mastitis isolates to identify factors involved in mastitis severity. Methods and findings: We combined three “omic” approaches to comprehensively compare two clonally related S. aureus strains that were isolated from and shown to reproducibly induce severe (strain O11) and milder (strain O46) mastitis in ewes. The genomes of O11 and O46 were sequenced (Illumina technology) to determine their respective gene content and comparative transcriptomic and proteomic analyses were carried out on both strains grown in conditions mimicking mastitis context. High differences were highlighted in mobile genetic elements, iron acquisition and metabolism, transcriptional regulation and exoprotein production. In particular, O11 overproduced exoproteins, including toxins and proteases when compared to O46. This was confirmed in 4 other S. aureus strains isolated from subclinical or clinical mastitis cases. Dose-dependant production of some staphylococcal factors seem to play a role in hypervirulence of strains isolated from severe mastitis. Mobile genetic elements, transcriptional regulators, exoproteins or strain ability to deal with iron starvation constitute good targets for further research to better define the underlying mechanisms of mastitis severity. Conclusions: Differences observed in mastitis severity likely result from the ability of the strains to adapt and to express virulence factors in the mastitis context rather than from deep variations in gene content. Expression of S. aureus O46 from subclinical mastitis and O11 from a lethal gangrenous mastitis were compared at two different times
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Project description:Sensing of microbial products by innate immune cells skew their transcriptional program to optimize anti-microbial defences. Chromatin remodeling by histone deacetylases (HDACs) plays a fundamental role in tailoring gene expression. HDAC inhibitors are among the most promising anti-cancer drugs and possess intrinsic anti-inflammatory properties. Yet, the influence of HDAC inhibition on innate immune responses to microbial infection is unknown. Here we show that HDAC inhibitors repress the expression of less than 10% of the genes expressed at baseline in BM-derived macrophages. In sharp contrast, HDAC inhibitors strongly interfere with transcriptome remodeling induced by LPS and Pam3CSK4, affecting the expression of 30-70% of genes modulated by microbial stimuli. Strikingly, HDAC inhibitors target the expression of numerous genes involved in anti-microbial host defences, encoding for microbial sensors, cytokines, chemokines, growth factors and their receptors, adhesion and signaling molecules, and molecules involved in antigen processing and presentation. At the molecular level, HDAC inhibitors do not impair mitogen-activated protein kinase, NF-kB, interferon-related factor signal and STAT1 transduction pathways, but inhibit NF-kB p65 recruitment to the promoter region of HDAC inhibitor-sensitive genes. HDAC inhibitors also inhibit the response of mouse and human DCs, splenocytes and whole blood to a broad range of microbial products and microorganisms. In agreement with these in vitro findings, HDAC inhibitors increase bacterial burden and sensitize mice to sub-lethal infection with Klebsiella pneumoniae and Candida albicans. Conversely, HDAC inhibitors confer protection in models of Pam3CSK4-induced fulminant toxic shock and severe sepsis following cecal ligation and puncture. Overall, these data substantiate the concept of immunomodulation by HDAC inhibitors, and suggest that these drugs could represent efficacious adjunctive therapy of severe sepsis. Mus musculus cells were grown in presence of LPS or LPS + TSA and pam or pam + TSA and hybrydised against a cRNA pool UMRR (from Mus musculus cells).
2011-01-01 | E-GEOD-22409 | biostudies-arrayexpress
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