ABSTRACT: EMG produced TPA metagenomics assembly of PRJNA777294 data set (Tracking Genomic Characteristics across Oceanic Provinces: Contrasting Early and Mature Plastic Biofilm Communities).
Project description:Several environmental bacteria encode plastic-degrading enzymes, a potential evolutionary response to the rapid introduction of plastic across global ecosystems. Given the widespread use of plastic in healthcare, we hypothesised that clinical bacterial isolates may also degrade plastic, rendering plastic-containing medical devices susceptible to degradation and failure and potentially offering these pathogens a carbon source that could be used to persist in the hospital-built environment. Here, we mined the genomes of prevalent pathogens and identified several enzymes in different pathogens with homology to known plastic-degrading enzymes. Synthesising and expressing a potential plastic-degrading enzyme derived from a Pseudomonas aeruginosa wound isolate in a heterologous host, we were able to demonstrate potent plastic degrading activity. We subsequently found that the original P. aeruginosa clinical isolate could reduce the weight of a medically relevant plastic, polycaprolactone (PCL), by 78% in 7 days, and critically could use it as a sole carbon source to grow. We uncovered a direct link to virulence, demonstrating that encoding a plastic degrading enzyme can significantly enhance biofilm formation and pathogenicity in vivo. We also demonstrate that this augmented biofilm phenotype is conserved in another P. aeruginosa PCL-degrading clinical isolate we identified in a screening. We reveal that the mechanism underpinning this enhanced biofilm formation is the incorporation of the plastic breakdown products into the extracellular matrix, leading to enhanced biofilm levels. The level of PCL degradation we show by a clinical isolate and its ability to promote a key virulence and persistence determinant such as biofilm formation indicates that the integrity of any PCL containing medical device, such as sutures or implants, and the condition of patients receiving such devices could be severely compromised by pathogens with this capacity. Given the central role of plastic in healthcare, this should be considered in the future of medical interventions and practice and hospital designs implementing this material
Project description:Aspergillus fumigatus is a filamentous fungus found in compost and soil that can cause invasive and/or chronic disease in a broad spectrum of individuals. Diagnosis and treatment of aspergillosis often occur during stages of infection when A. fumigatus has formed dense networks of hyphae within the lung. These dense hyphal networks are multicellular, encased in a layer of extracellular matrix, and have reduced susceptibility to contemporary antifungal drugs, characteristics which are defining features of a microbial biofilm. A mode of growth similar to these dense hyphal networks observed in vivo can be recapitulated in vitro using a static, submerged biofilm culture model. The mechanisms underlying filamentous fungal cell physiology at different stages of biofilm development remain to be defined. Here, we utilized an RNA sequencing approach to evaluate changes in transcript levels during A. fumigatus biofilm development. These analyses revealed an increase in transcripts associated with fermentation and a concomitant decrease in oxidative phosphorylation related transcripts. Further investigation revealed that ethanol and butanediol fermentation is important for mature biofilm biomass maintenance. Correspondingly, a gene (silG), a predicted transcription factor, was observed to also be required for mature biofilm biomass maintenance. Taken together, these data suggest temporal changes in A. fumigatus metabolism during biofilm development are required to maintain a fully mature biofilm.
2025-06-03 | GSE298422 | GEO
Project description:EMG produced TPA metagenomics assembly of PRJEB15404 data set (Plastic Metagenome Study).
Project description:Optimisation of DNA-protein co-extraction from the thin microbial biofilm inhabiting marine plastic debris for meta-omics and comparative metaproteomics analysis.
Project description:Salmonella spp. biofilms have been implicated in persistence in the environment and plant surfaces. In addition, Salmonella is able to form biofilms on the surface on cholesterol gallstones. The ability of Salmonella spp. on these surfaces is superior to biofilm formation on surfaces on glass or plastic. Thus, we hypothesized that Salmonella gene expression is specific during biofilm development on cholesterol surfaces.
Project description:The authors of this manuscript suggest the stoichiometry of outer submodules of the budding yeast kinetochore is strongly influenced by factors at the kinetochore-microtubule interface, including Fin1, Dam1, and microtubule tracking. Outer kinetochore stoichiometry is remarkably plastic and responsive to microtubule-proximal regulation.
Project description:Starvation in diploid budding yeast cells triggers a cell-fate program culminating in meiosis and spore formation. Transcription activation of early meiotic genes (EMGs) hinges on the transcription activator Ime1, its DNA-binding partner Ume6, and GSK-3 kinase Rim11. Phosphorylation of Ume6 by Rim11 is key for EMG activation. We report that Rim11 functions as the central signal integrator for controlling Ume6 phosphorylation and EMG transcription. In nutrient-rich conditions, PKA suppresses Rim11 levels, while TORC1 retains Rim11 in the cytoplasm. Inhibiting PKA and TORC1 induces Rim11 expression and nuclear localization. Remarkably, nuclear Rim11 is required, but not sufficient, for Rim11-dependent Ume6 phosphorylation. Additionally, Ime1 is an essential anchor protein for phosphorylating Ume6. Subsequently, Ume6-Ime1 coactivator complexes form, which drive EMG transcription. Our results demonstrate how varied signalling inputs (PKA/TORC1/Ime1) converge through Rim11 to regulate EMG expression and meiosis initiation. We posit that the signalling-regulatory network elucidated here generates robustness in cell-fate control.