microLife

Patients with Crohns disease exhibit abnormal colonization of the intestine by proteobacteria, and among these bacteria, the adherent invasive E. coli (AIEC) family. They are predominant in the mucus, adhere to epithelial cells, colonize them and survive inside macrophages. We recently demonstrated that the acclimation of the AIEC strain LF82 to phagolysosomal stress requires stringent and SOS responses. Such adaptation involves a long lag phase in which many LF82 cells become antibiotic tolerant. Later during infection, they proliferate in vacuoles and form colonies harboring dozens of LF82 bacteria. In the present work, we investigated the mechanism sustaining this phase of growth. We found that intracellular LF82 produced an extrabacterial matrix composed of exopolysaccharides and amyloid fibers that surrounded each individual LF82 cell. This matrix acts as a biofilm and controls the formation of LF82 intracellular bacterial communities (IBCs) inside phagolysosomes for several days post infection. Using genomics assays, we characterized the gene set involved in IBCs formation and revealed the crucial role played by a pathogenicity island presents in the genome of most AIEC strains in this process. Iron capture, by the yersiniabactin system encoded by this pathogenicity island, is essential to form IBC and LF82 survival within macrophages. These results demonstrate that AIEC have developed a sophisticated strategy to establish their replicative niche within macrophages, which might have implications for envisioning future antibacterial strategies for Crohns disease.

Bacteria can rapidly tune their physiology and metabolism to adapt to environmental fluctuations. In particular, they can adapt their lifestyle to the close proximity of other bacteria or presence of different surfaces. However, whether these interactions trigger transcriptomic responses is poorly understood. We used a specific set up of E. coli strains expressing native or synthetic adhesins mediating bacterial aggregation to study the transcriptomic changes of aggregated compared to non-aggregated bacteria. Our results show that following aggregation, bacteria exhibit a core response independent of the adhesin type, with differential expression of 56.9% of the coding genome, including genes involved in stress response and anaerobic lifestyle. Moreover, when aggregates were formed via a naturally expressed E. coli adhesin (Antigen 43), the transcriptomic response of the bacteria was more exaggerated compared to aggregates formed via a synthetic adhesin. This suggests that the response to aggregation induced by native E. coli adhesins could have been finely tuned during bacterial evolution. Our study therefore provides insights on the effect of self-interaction in bacteria and allows a better understanding of why bacterial aggregates exhibit increased stress tolerance. ImportanceFormation of bacterial aggregates has an important role in both clinical and ecological contexts. Although these structures have been previously shown to be more resistant to stressful conditions, the genetic basis of this stress tolerance associated with the aggregate lifestyle is poorly understood. Surface sensing mediated by different adhesins can result in varying changes on bacterial physiology. However, whether adhesin-adhesin interactions as well as the type of adhesin mediating aggregation affects bacterial cell physiology is unknown. By sequencing the transcriptomes of aggregated and non-aggregated cells expressing native or synthetic adhesins, we characterized the effects of aggregation and adhesin type on E. coli physiology.

CRISPR-Cas systems in prokaryotes utilize spacers, segments of DNA acquired from invading phages, to guide immune defense mechanisms. This study investigates the evolution of CRISPR repertoire size by examining its relationships with repeat length, terminal repeat polymorphism, and structural stability in 1,958 bacterial genomes, identifying 5,465 CRISPR arrays. Using CRISPRCasFinder for annotation and RNAfold for predicting RNA secondary structures, we found significant variation in array characteristics. Long-repeat arrays ([&ge;]38 bp) showed a significant positive correlation between terminal repeat polymorphism and CRISPR spacer number, a correlation absent in short-repeat arrays (<38 bp), suggesting longer repeats facilitate recombination and spacer loss. Additionally, a negative correlation between repeat length and spacer number across all arrays indicates that longer repeats may accelerate spacer loss. Furthermore, our results show that immune demand significantly influences the evolution of spacer number. Larger CRISPR repertoires correlate with conserved repeat sequences and stable secondary structures, vital for functional arrays under continuous selective pressure. Comparing functional and obsolete CRISPR arrays (orphan arrays in genomes lacking Cas genes) revealed that obsolete arrays have fewer spacers and lower repeat consistency, indicating a degenerative state. By elucidating the factors that shape CRISPR memory size evolution, this research offers strategies to enhance bacterial defenses, mitigate resistance, and improve applications in gene editing and therapeutics.

Cellulose is a major component of the Salmonella biofilm extracellular matrix and it is considered an antivirulence factor because it interferes with Salmonella survival inside macrophages and virulence in mice. Its synthesis is stimulated by CsgD, the master regulator of biofilm extracellular matrix formation in enterobacteria, which in turn is under the control of MlrA, a MerR-like transcription factor. In this work we identified a SPI-2 encoded Salmonella-specific transcription factor homolog to MlrA, MlrB, that represses transcription of its downstream gene, STM1389, also known as orf319, and of csgD inside host cells. MlrB is induced in laboratory media mimicking intracellular conditions and inside macrophages, and it is required for intramacrophage survival. An increased expression of csgD is observed in the absence of MlrB inside host cells. Interestingly, inactivation of the CsgD-controlled cellulose synthase coding-gene, bcsA, restored intramacrophage survival to rates comparable to wild type bacteria in the absence of MlrB. These data indicate that MlrB represses CsgD expression inside host cells and in consequence activation of the cellulose synthase. Our findings provide a novel link between biofilm formation and Salmonella virulence.

Lipopolysaccharide is essential for most Gram-negative bacteria as it is a main component of the outer membrane. In the pathogen Brucella abortus, smooth lipopolysaccharide containing the O-antigen is required for virulence. Being part of the Rhizobiales, Brucella spp. display unipolar growth and lipopolysaccharide was shown to be incorporated at the active growth sites, i.e. the new pole and the division site. By localizing proteins involved in the lipopolysaccharide transport across the cell envelope, from the inner to the outer membrane, we show that the lipopolysaccharide incorporation sites are determined by the inner membrane complex of the lipopolysaccharide transport system. Moreover, we identify the main O-antigen ligase of Brucella spp involved in smooth lipopolysaccharide synthesis. Altogether, our data highlight a new layer of spatiotemporal organization of the lipopolysaccharide biosynthesis pathway and identify a new class of bifunctional O-antigen ligases.

CRISPR-Cas systems are best known for their role in adaptive immunity, but emerging evidence suggests broader regulatory functions. Here, we show that the CRISPR-Cas system acts as a serovar-specific regulator of stress adaptation in Salmonella enterica, exerting opposing effects in host-restricted (S. Typhi) and broad-host-range (S. Typhimurium) serovars. In S. Typhi, CRISPR-Cas system deletion reduces acid and bile tolerance by impairing envelope integrity and repressing key stress-response regulators (envZ, cadB, phoPQ, lexA, ruvB, wecD), while increasing resistance to cationic antimicrobial peptides via pmr activation and reduced oxidative damage. Conversely, CRISPR-Cas system loss in S. Typhimurium enhances acid survival-partly through speF upregulation but increases sensitivity to antimicrobial peptides. Spacer-1 of S. Typhi CRISPR-I array as the main regulator of gene expression, and its reintroduction partially restored stress tolerance, supporting spacer-dependent control of physiological pathways. These findings establish the CRISPR-Cas system as a non-canonical, spacer-dependent regulator of stress response networks in S. enterica, revealing its contribution to the evolutionary divergence of survival strategies between S. Typhi and S. Typhimurium.

Patients with Crohns disease exhibit abnormal colonization of the intestine by Proteobacteria, particularly the adherent-invasive Escherichia coli (AIEC) group. These bacteria are predominant in the mucus, adhere to epithelial cells, colonize them, and survive inside macrophages. We recently demonstrated that the acclimation of strain LF82 to phagolysosomal stress occurs in two distinct steps: first, a replication halt producing stress- tolerant persisters, and second, a replication phase that leads to the formation of Intracellular Bacterial Communities (IBC) organized with a biofilm-like matrix. Given the significant genomic diversity among strains with the AIEC phenotype, we conducted a comparative analysis of the genomes and macrophage colonization characteristics of 13 AIEC strains collected from patients during a clinical study conducts by the CHU of Clermont-Ferrand. Our results demonstrate that IBCs serve as replicative niches for all AIEC strains within macrophages. However, these strains form IBCs using different strategies, including varying levels of phagosome detoxification, distinct biofilm characteristics, and diverse macrophage responses. Our study reveals a strong positive correlation between vacuole acidification and persister induction that explains intracellular survival of the different strains. In addition, we revealed distinct AIEC dissemination strategies outside macrophages, which may contribute to the propagation of inflammation in the human host. These findings highlight that research on pathogens and pathobionts with plastic genomes should not rely solely on a few laboratory models.

The bacterial cell envelope is an essential structure that protects the cell from environmental threats, while simultaneously serving as communication interface and diffusion barrier. Therefore, maintaining cell envelope integrity is of vital importance for all microorganisms. Not surprisingly, evolution has shaped conserved protection networks that connect stress perception, transmembrane signal transduction and mediation of cellular responses upon cell envelope stress. The phage shock protein (PSP) stress response is one of such conserved protection networks. Most of the knowledge about the Psp response comes from studies in the Gram-negative model bacterium, Escherichia coli where the Psp system consists of several well-defined protein components. Homologous systems were identified in representatives of Proteobacteria, Actinobacteria, and Firmicutes; however, the Psp system distribution in the microbial world remains largely unknown. By carrying out a large-scale, unbiased comparative genomics analysis, we found components of the Psp system in many bacterial and archaeal phyla and demonstrated that the PSP system deviates dramatically from the proteobacterial prototype. Two of its core proteins, PspA and PspC, have been integrated in various (often phylum-specifically) conserved protein networks during evolution. Based on protein sequence and gene neighborhood analyses of pspA and pspC homologs, we built a natural classification system of PSP networks in bacteria and archaea. We performed a comprehensive in vivo protein interaction screen for the PSP network newly identified in the Gram-positive model organism Bacillus subtilis and found a strong interconnected PSP response system, illustrating the validity of our approach. Our study highlights the diversity of PSP organization and function across many bacterial and archaeal phyla and will serve as foundation for future studies of this envelope stress response beyond model organisms.

Iron is essential for bacterial growth but can be toxic in excess. To maintain iron homeostasis, bacteria employ regulatory mechanisms, including small RNAs (sRNAs). In Staphylococcus aureus, we identified the sRNA IsrR as a critical mediator of the iron-sparing response, enabling bacterial fitness in iron-limited environments such as those encountered during host infection. Here, we use ribosome profiling (Ribo-seq) to define the translational regulatory network of IsrR under iron-limited conditions. Our analysis identifies multiple genes under IsrR control, including SAOUHSC_02924 (gabT), which encodes a putative 4-aminobutyrate aminotransferase. Given that IsrR downregulates iron-dependent TCA cycle enzymes, we propose that repression of gabT prevents the accumulation of TCA cycle precursors under iron depletion, thereby avoiding metabolic imbalances. These findings expand the role of IsrR in metabolic reprogramming and highlight its contribution to S. aureus survival in iron-restricted host niches.

Natural competence for genetic transformation, considered as one of the three main mechanisms leading to horizontal gene transfer in bacteria, is able to promote evolution, through genomic plasticity, and foster antibiotic resistance and virulence factors spreading. Conserved machineries and actors required to perform genetic transformation have been shown to accumulate at different cellular localizations depending on the model organism considered. Here, we show in the human pathogen Staphylococcus aureus that DNA binding, uptake and recombination are spatially and temporally coordinated to ensure S. aureus genetic transformation. We also reveal that localization of genetic transformation proteins is dynamic and preferentially occurs in the vicinity of the division septum. We finally propose that S. aureus competent cells would initiate and then block cell division to ensure the success of genetic transformation before the final constriction of the cytokinetic ring.

NLRs (Nod-like receptors) are intracellular receptors regulating immunity, symbiosis, non-self recognition and programmed cell death in animals, plants and fungi. Several fungal NLRs employ amyloid signaling motifs to activate downstream cell-death inducing proteins. Herein, we identify in Archaea and Bacteria, short sequence motifs that occur in the same genomic context as fungal amyloid signaling motifs. We identify 10 families of bacterial amyloid signaling sequences (we term BASS), one of which (BASS3) is related to mammalian RHIM and fungal PP amyloid motifs. We find that BASS motifs occur specifically in bacteria forming multicellular structures (mainly in Actinobacteria and Cyanobacteria). We analyze experimentally a subset of these motifs and find that they behave as prion forming domains when expressed in a fungal model. All tested bacterial motifs also formed fibrils in vitro. We analyze by solid-state NMR and X-ray diffraction, the amyloid state of a protein from Streptomyces coelicolor bearing the most common BASS1 motif and find that it forms highly ordered non-polymorphic amyloid fibrils. This work expands the paradigm of amyloid signaling to prokaryotes and underlies its relation to multicellularity.

CRISPR-Cas systems endow bacteria and archaea with adaptive immunity against mobile genetic elements, playing a fundamental role in shaping microbial communities. Many organisms harbor more than one CRISPR-Cas system, and little is known about whether and how they are differentially regulated, in many instances due to the impossibility of studying CRISPR immunity in native hosts. Here we studied the regulation of endogenous type II-B and type V-A CRISPR-Cas systems in opportunistic human pathogen Francisella novicida U112. Fluorescence microscopy and transcriptomics experiments revealed that while the type II-B system is constitutively expressed, the type V-A CRISPR-Cas system is differentially expressed at stationary phase and high cell density. Using mass spectrometry and genetics we identified MtvS as a factor required for the differential expression of the type V-A CRISPR-Cas locus. Surprisingly, MtvS-dependent expression of the type V-A CRISPR-Cas system at high cell density is linked to a quorum sensing-like behavior. In addition, MtvS modulates transcription of many genes in stationary phase, some of which are required for Francisella virulence. Pull-down experiments revealed MtvS interacts with the {beta} subunit of the RNA polymerase and therefore may constitute a noncanonical alternative sigma factor involved in the regulation of the expression of CRISPR loci and other genes.

Archaea and bacteria routinely live side by side in microbial communities and must interact at least on occasion. Whether such cross-Domain interactions are dominated by mutual disregard, co-operation, or conflict remains fundamentally unknown. One potential window into archaeal-bacterial conflict is to ask whether some of the molecular weapons bacteria wield to kill other bacteria are present in archaea, and vice versa. Here, to start to address this question, we carry out a phylogenomic survey of bacteriocins in archaeal genomes and archaeocins in bacterial genomes. We find that more than 20% of known bacteriocins - proteins deployed by bacteria against other bacteria - have at least one homolog in archaea. Typically, these archaeal homologs are related to bacteriocins targeting (and encoded by) monoderm bacteria. Based on conservation of functionally critical residues, protein structure, and accessory genes critical for bacteriocin biosynthesis, we highlight homologs of subtilosin A, encoded in some Thermococcus archaea, as promising candidates for experimental follow- up work. We also show that halocin C8, originally described in Natrinema archaea, is comparatively common in bacterial genomes, including a number of skin-resident Staphylococcus species. Our results suggest that bacteriocins/archaeocins are shared across Domain boundaries with some regularity. While many instances are phylogenetically isolated - raising doubts about their functional importance and integration into host physiology - some bacteriocins are present in multiple related genomes and embedded in broader biosynthetic gene clusters that are also found in the original producers, suggesting that archaea and bacteria periodically use the same weapon systems in conflicts with other microbes. Further study of these systems might elucidate cross-Domain conflict and the nature of archaeal-bacterial interactions in different environments.

In prokaryotes, CRISPR-Cas systems store memories of past infections in the form of spacers integrated into CRISPR arrays. When associated with type III CRISPR-Cas systems, Reverse transcriptase-Cas1 fusion proteins (RT-Cas1) enable these defense systems to acquire spacers from RNA sources. However, despite the specific targeting of RNA by the Cas13-containing type VI CRISPR-Cas systems, there is no evidence of RNA-origin spacer acquisition. Using computational analyses, we recently reported the association of RT-Cas1 fusion proteins with type VI-A systems. In this study, we found that RT-Cas1 fusion proteins were also associated with complete type VI-B systems in bacteria from gut metagenomes, constituting a variant system that harbors a linked CorA-encoding locus in addition to the CRISPR array and adaptation RT-Cas1/Cas2 module. By combining in vitro and in vivo experiments, we demonstrated that type VI RT-CRISPR systems are functional for spacer acquisition and CRISPR array processing, and that the associated RT enables spacer acquisition from RNA molecules, thus demonstrating that the system is capable of functioning independently of other in-trans systems. These findings highlight the importance of RTs in RNA-targeting CRISPR-Cas systems, suggesting a potential defense mechanism against RNA-based invaders in specific environments.

Salmonella enterica serovar Infantis (SIN) has rapidly become the dominant serovar in poultry worldwide, a success largely linked to the acquisition of the 285 kb megaplasmid pESI. While pESI-encoded antibiotic-resistance and iron-uptake systems are well characterized, pESI-mediated adhesion mechanisms remain poorly understood. Here we identify a novel pESI-encoded monomeric autotransporter adhesin, designated PeaP (pESI-encoded autotransporter protein), and demonstrate its pivotal role in atypical biofilm formation, interference with motility, and colonization of the chicken host. Biofilm assays revealed that pESI-harboring strain SIN 119944 forms robust biofilms at 37 {degrees}C and 42 {degrees}C, temperatures at which CsgD-dependent biofilm formation is negligible. Deletion of csgD did not impair this phenotype, whereas deletion of peaP abolished high-temperature biofilm development and restored motility to wild-type levels. Proteomic profiling of sessile versus planktonic cells highlighted PeaP as the most abundant pESI-derived protein in the biofilm fraction. AlphaFold-based modelling and negative-stain transmission electron microscopy showed that PeaP comprises a C-terminal {beta}-barrel and a 1,500 aa passenger domain with three tandem repeats, projecting filamentous appendages [~]37 nm from the outer membrane. Antibody blockade of PeaP reduced surface adhesion >6-fold, confirming its adhesive function. In an infection model of 2 day-old chicken, the peaP mutant displayed significantly lower colonization, indicating PeaP-mediated adhesion in vivo. Collectively, pESI-positive SIN deploys PeaP for CsgD-independent, temperature-tolerant biofilm formation and enhanced gastrointestinal colonization, providing a mechanistic basis for the epidemic spread of this multidrug-resistant pathogen in poultry.

In bacteria, transcription and RNA degradation are physically separated via segregation of the main ribonucleolytic machinery - the RNA degradosome - into phase-separated or membrane-anchored molecular assemblies driven by RNase E. Despite the widespread conservation of an amphipathic membrane anchor (MTS) in RNase E, the regulatory information embedded within this sequence and its biological importance remain poorly understood. Here, we have studied the importance of the Pseudomonas aeruginosa RNase E MTS for bacterial fitness or virulence and assessed its interchangeability. We show that amphipathicity is dispensable for foci scaffolding but necessary for proper foci morphology, dynamics, and localisation, although sequence modulates foci behaviour. Loss of the MTS additionally causes a drastic sensitivity to high salinity and a consistent virulence defect in Galleria mellonella larvae. Moreover, transcriptomics and analysis of mRNA spatial organisation reveal that the MTS mutant has specific stabilisation of localised membrane protein-encoding transcripts, together with abnormal operon processing. Altogether, our study highlights the elegant MTS-mediated control of spatial organisation and target selection, shaping the transcriptome and bacterial stress response.

Effector translocation during host-pathogen interactions is a prerequisite for the entry of Salmonella into non-phagocytic cells and establishment of a replication permissive intracellular niche. Deciphering the dynamics and kinetics of translocation and subcellular localization demands live-cell imaging and tagging approaches that do not introduce detection delays or perturb the translocation process via the type III secretion system (T3SS). Effector fusions with self-labelling enzymes (SLE), such as HaloTag, allow localization and tracking at high temporal and spatial resolution. However, interference with T3SS-dependent translocation has hampered analyses of the process of translocation and early subcellular distribution and dynamics. Herein, we report that amino acid substitutions of the HaloTag can reduce the thermodynamic stability, resulting in less steric hindrance during translocation of effector-HaloTag fusions by the T3SS in mammalian cells. The top variant, HT-SP5, showed reduced retention in Salmonella, enabling more sensitive and earlier detection of translocated effector proteins of the SPI1 and SPI2 T3SS of Salmonella and of the T3SS effector Map of enteropathogenic Escherichia coli (EPEC). We applied the improved HaloTag HT-SP5 to single molecule tracking, and to follow effector protein dynamics in living host cells early after translocation by invading and intracellular bacteria. Taken together, the improved HaloTag variant HT-SP5 represents a robust and versatile SLE tag for dynamic real-time analyses of delivery and fate of T3SS-translocated effector proteins in living cells host. Application of HT-SP5 will facilitate research on effectors throughout the entire infection process at native effector levels to understand host-pathogen interactions.

Type VI secretion systems (T6SS) are common bacterial contractile injection systems that inject toxic "effector" proteins into neighboring cells. Effector discovery is generally done manually, and computational approaches used for effector discovery depend on genetic linkage to T6SS genes and/or sequence similarity to known effectors. We bioinformatically investigated T6SS in more than 11,832 genomes of Gram negative bacteria. We found that T6SS encoding bacteria are host-associated and pathogenic, enriched in specific human and plant tissues, while depleted in marine, soil, and engineered environments. Analysis of T6SS cores with C-terminal domains ("evolved" cores) showed "evolved" HCP are rare, overwhelmingly encoded in orphan operons, and are largely restricted to Escherichia. Using the wealth of data generated from our bioinformatic analysis, we developed two algorithms for large-scale discovery of T6SS effector proteins (T6Es). We experimentally validated ten putative antibacterial T6SS effector proteins and one cognate immunity gene from a diverse species. This study provides a systematic genomic perspective of the role of the T6SS in nature, a thorough analysis of T6E evolution and genomic properties, and discovery of a large number of candidate T6Es using new approaches.

The type VI secretion system (T6SS) is a contact-dependent contractile multiprotein apparatus widely distributed in Gram-negative bacteria. These systems can deliver different effector proteins into target bacterial and/or eukaryotic cells, contributing to the environmental fitness and virulence of many bacterial pathogens. Salmonella harbors five different T6SSs encoded in different genomic islands. The T6SS encoded in Salmonella Pathogenicity Island 6 (SPI-6) contributes to Salmonella competition with the host microbiota and its interaction with infected host cells. Despite its relevance, information regarding the total number of effector proteins encoded within SPI-6 and its distribution among different Salmonella enterica serotypes is limited. In this work, we performed bioinformatic and comparative genomics analyses of the SPI-6 T6SS gene cluster to expand our knowledge regarding the T6SS effector repertoire and the global distribution of these effectors in Salmonella. The analysis of a curated dataset of 60 Salmonella enterica genomes from the Secret6 database revealed the presence of 23 novel putative T6SS effector/immunity protein (E/I) modules. These effectors were concentrated in the variable regions 1 to 3 (VR1-3) of the SPI-6 T6SS gene cluster. VR1-2 were enriched in candidate effectors with predicted peptidoglycan hydrolase activity, while VR3 was enriched in candidate effectors of the Rhs family with C-terminal extensions with predicted DNase, RNase, deaminase, or ADP-ribosyltransferase activity. A global analysis of known and candidate effector proteins in Salmonella enterica genomes from the NCBI database revealed that T6SS effector proteins are differentially distributed among Salmonella serotypes. While some effectors are present in over 200 serotypes, others are found in less than a dozen. A hierarchical clustering analysis identified Salmonella serotypes with distinct profiles of T6SS effectors and candidate effectors, highlighting the diversity of T6SS effector repertoires in Salmonella enterica. The existence of different repertoires of effector proteins suggests that different effector protein combinations may have a differential impact on the environmental fitness and pathogenic potential of these strains.

Iron is an essential nutrient for microbial growth. The opportunistic pathogen Pseudomonas aeruginosa can survive under diverse conditions, including iron-depleted environments with the aid of small non-coding RNAs (sRNAs). P. aeruginosa also uses three quorum sensing (QS) systems Las, Rhl, and Pqs to coordinate virulence and infection establishment at the population level. This study links the sRNA Lrs1, which is located within the promoter of the Pqs biosynthetic operon pqsABCDE, to iron uptake regulation in the P. aeruginosa strain PAO1-L. Transcriptomics and phenotypic assays indicate that Lrs1 downregulates the production of the siderophore pyochelin but not pyoverdine, and that lrs1 regulation itself is dependent on iron availability. Although Lrs1 has been implicated in a positive feedback loop with the transcriptional regulator LasR in the strain PA14, the present findings indicate that this is not the case in PAO1-L in the tested conditions. Transcription of Lrs1 is dependent on quorum sensing, predominantly on RhlR with an auxiliary effect by PqsE. Furthermore, the Pqs system and phenazine production are modulated by Lrs1 only under iron limitation. This study identifies Lrs1 as a new QS-dependent post-transcriptional regulator of iron uptake and virulence highlighting its importance in environmental adaptation in P. aeruginosa. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=74 SRC="FIGDIR/small/627364v1_ufig1.gif" ALT="Figure 1"> View larger version (12K): org.highwire.dtl.DTLVardef@1585ca5org.highwire.dtl.DTLVardef@2a7d55org.highwire.dtl.DTLVardef@18a712eorg.highwire.dtl.DTLVardef@c84d2_HPS_FORMAT_FIGEXP M_FIG C_FIG