On the origin of [Ne II] emission in young stars: mid-infrared and optical observations with the Very Large Telescope

{Abridged version for ArXiv}. We provide direct constraints on the origin of the [Ne II] emission in 15 young stars using high-spatial and spectral resolution observations with VISIR at the VLT that allow us to study the kinematics of the emitting gas. In addition we compare the [Ne II] line with optical forbidden lines observed for three stars with UVES. The [Ne II] line was detected in 7 stars, among them the first confirmed detection of [Ne II] in a Herbig Be star, V892 Tau. In four cases, the large blueshifted lines indicate an origin in a jet. In two stars, the small shifts and asymmetric profiles indicate an origin in a photo-evaporative wind. CoKu Tau 1, seen close to edge-on, shows a spatially unresolved line centered at the stellar rest velocity, although cross-dispersion centroids move within 10 AU from one side of the star to the other as a function of wavelength. The line profile is symmetric with wings extending up to about +-80 km/s. The origin of the [Ne II] line could either be due to the bipolar jet or to the disk. For the stars with VLT-UVES observations, in several cases, the optical forbidden line profiles and shifts are very similar to the profile of the [Ne II] line, suggesting that the lines are emitted in the same region. A general trend observed with VISIR is a lower line flux when compared with the fluxes obtained with Spitzer. We found no correlation between the line full-width at half maximum and the line peak velocity. The [Ne II] line remains undetected in a large part of the sample, an indication that the emission detected with Spitzer in those stars is likely extended.Comment: Accepted for publication in Astronomy & Astrophysics; revised version: corrected minor typos, corrected center values (col 3) for CoKuTau1 in Table

TADB: a web-based resource for Type 2 toxin–antitoxin loci in bacteria and archaea

TADB (http://bioinfo-mml.sjtu.edu.cn/TADB/) is an integrated database that provides comprehensive information about Type 2 toxin–antitoxin (TA) loci, genetic features that are richly distributed throughout bacterial and archaeal genomes. Two-gene and much less frequently three-gene Type 2 TA loci code for cognate partners that have been hypothesized or demonstrated to play key roles in stress response, bacterial physiology and stabilization of horizontally acquired genetic elements. TADB offers a unique compilation of both predicted and experimentally supported Type 2 TA loci-relevant data and currently contains 10 753 Type 2 TA gene pairs identified within 1240 prokaryotic genomes, and details of over 240 directly relevant scientific publications. A broad range of similarity search, sequence alignment, genome context browser and phylogenetic tools are readily accessible via TADB. We propose that TADB will facilitate efficient, multi-disciplinary and innovative exploration of the bacteria and archaea Type 2 TA space, better defining presently recognized TA-related phenomena and potentially even leading to yet-to-be envisaged frontiers. The TADB database, envisaged as a one-stop shop for Type 2 TA-related research, will be maintained, updated and improved regularly to ensure its ongoing maximum utility to the research community

Bacterial Toxin–Antitoxin Systems: More Than Selfish Entities?

Bacterial toxin–antitoxin (TA) systems are diverse and widespread in the prokaryotic kingdom. They are composed of closely linked genes encoding a stable toxin that can harm the host cell and its cognate labile antitoxin, which protects the host from the toxin's deleterious effect. TA systems are thought to invade bacterial genomes through horizontal gene transfer. Some TA systems might behave as selfish elements and favour their own maintenance at the expense of their host. As a consequence, they may contribute to the maintenance of plasmids or genomic islands, such as super-integrons, by post-segregational killing of the cell that loses these genes and so suffers the stable toxin's destructive effect. The function of the chromosomally encoded TA systems is less clear and still open to debate. This Review discusses current hypotheses regarding the biological roles of these evolutionarily successful small operons. We consider the various selective forces that could drive the maintenance of TA systems in bacterial genomes

Ciprofloxacin Causes Persister Formation by Inducing the TisB toxin in Escherichia coli

Persisters are specialized survivor cells that arise in populations of E. coli after antibiotic-mediated DNA damage induces the production of a small membrane-acting peptide TisB, which causes reversible dormancy. The TisB-dependent persisters are tolerant to multiple antibiotics

The relBE2Spn Toxin-Antitoxin System of Streptococcus pneumoniae: Role in Antibiotic Tolerance and Functional Conservation in Clinical Isolates

Type II (proteic) chromosomal toxin-antitoxin systems (TAS) are widespread in Bacteria and Archaea but their precise function is known only for a limited number of them. Out of the many TAS described, the relBE family is one of the most abundant, being present in the three first sequenced strains of Streptococcus pneumoniae (D39, TIGR4 and R6). To address the function of the pneumococcal relBE2Spn TAS in the bacterial physiology, we have compared the response of the R6-relBE2Spn wild type strain with that of an isogenic derivative, ΔrelB2Spn under different stress conditions such as carbon and amino acid starvation and antibiotic exposure. Differences on viability between the wild type and mutant strains were found only when treatment directly impaired protein synthesis. As a criterion for the permanence of this locus in a variety of clinical strains, we checked whether the relBE2Spn locus was conserved in around 100 pneumococcal strains, including clinical isolates and strains with known genomes. All strains, although having various types of polymorphisms at the vicinity of the TA region, contained a functional relBE2Spn locus and the type of its structure correlated with the multilocus sequence type. Functionality of this TAS was maintained even in cases where severe rearrangements around the relBE2Spn region were found. We conclude that even though the relBE2Spn TAS is not essential for pneumococcus, it may provide additional advantages to the bacteria for colonization and/or infection

ε/ζ systems: their role in resistance, virulence, and their potential for antibiotic development

Cell death in bacteria can be triggered by activation of self-inflicted molecular mechanisms. Pathogenic bacteria often make use of suicide mechanisms in which the death of individual cells benefits survival of the population. Important elements for programmed cell death in bacteria are proteinaceous toxin–antitoxin systems. While the toxin generally resides dormant in the bacterial cytosol in complex with its antitoxin, conditions such as impaired de novo synthesis of the antitoxin or nutritional stress lead to antitoxin degradation and toxin activation. A widespread toxin–antitoxin family consists of the ε/ζ systems, which are distributed over plasmids and chromosomes of various pathogenic bacteria. In its inactive state, the bacteriotoxic ζ toxin protein is inhibited by its cognate antitoxin ε. Upon degradation of ε, the ζ toxin is released allowing this enzyme to poison bacterial cell wall synthesis, which eventually triggers autolysis. ε/ζ systems ensure stable plasmid inheritance by inducing death in plasmid-deprived offspring cells. In contrast, chromosomally encoded ε/ζ systems were reported to contribute to virulence of pathogenic bacteria, possibly by inducing autolysis in individual cells under stressful conditions. The capability of toxin–antitoxin systems to kill bacteria has made them potential targets for new therapeutic compounds. Toxin activation could be hijacked to induce suicide of bacteria. Likewise, the unique mechanism of ζ toxins could serve as template for new drugs. Contrarily, inhibition of virulence-associated ζ toxins might attenuate infections. Here we provide an overview of ε/ζ toxin–antitoxin family and its potential role in the development of new therapeutic approaches in microbial defense

The human gut mobile metagenome: A metazoan perspective

Using the culture independent TRACA system in conjunction with a comparative metagenomic approach, we have recently explored the pool of plasmids associated with the human gut mobile metagenome. This revealed that some plasmids or plasmid families are present in the gut microbiomes of geographically isolated human hosts with a broad global distribution (America, Japan and Europe), and are potentially unique to the human gut microbiome. Functions encoded by the most widely distributed plasmid (pTRACA22) were found to be enriched in the human gut microbiome when compared to microbial communities from other environments, and of particular interest was the increased prevalence of a putative RelBE toxin-antitoxin (TA) addiction module. Subsequent analysis revealed that this was most closely related to putative TA modules from gut associated bacteria belonging to the Firmicutes, but homologues of the RelE toxin were associated with all major bacterial divisions comprising the human gut microbiota. In this addendum, functions of the gut mobile metagenome are considered from the perspective of the human host, and within the context of the hologenome theory of human evolution. In doing so, our original analysis is also extended to include the gut metagenomes of a further 124 individuals comprising the METAHIT dataset. Differences in the incidence and relative abundance of pTRACA22 and associated TA modules between healthy individuals and those with inflammatory bowel diseases are explored, and potential functions of pTRACA22 type RelBE modules in the human gut microbiome are discussed