Project description:The nitrogen rich compound guanidine occurs widely in nature and is used by microbes as a nitrogen source, but microorganisms that grow on guanidine have not yet been discovered. Here we show that complete ammonia-oxidizing microbes (comammox), but no other known nitrifiers, encode homologues of a guanidinase and that the comammox isolate Nitrospira inopinata grows on guanidine as sole source of energy and reductant. Proteomics, kinetic enzyme characterization, and the crystal structure of the N. inopinata guanidinase homologue demonstrated that it is a bona fide guanidinase. Transcription of comammox guanidinases was induced in wastewater treatment plant microbiomes upon incubation with guanidine, and guanidine degradation was detected in these systems. The discovery of guanidine as a selective growth substrate for comammox shows a unique niche of these globally important nitrifiers and offers new options for their isolation as well as for targeted manipulation of nitrifier communities.
2024-08-03 | PXD038826 | Pride
Project description:Enrichment of comammox with different nitrogen
Project description:Epigenetics is important in the pathogenesis of immune-mediated diseases like rheumatoid arthritis (RA). Here we show the first complete epigenomic characterization of RA fibroblast-like synoviocytes (FLS) by profiling histone modifications (H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K27me3, H3K9me3), open chromatin, RNA expression and whole genome DNA methylation. To address the complex multidimensional relationship and reveal the epigenetic regulation of RA, we perform integrative analyses using a novel unbiased method to identify genomic regions with similar profiles. Epigenomically similar regions exist in RA cells are particularly associated with active enhancers and promoters as well as specific transcription factor binding motifs. Differentially marked genes are enriched for immunological and unexpected pathways, with “Huntington's Disease Signaling” identified as particularly prominent. We validate the relevance of this pathway to RA by showing that Huntingtin-interacting protein-1 regulates FLS invasion into matrix. This work establishes a high-resolution epigenomic landscape of RA and demonstrates the potential for integrative analyses to identify unanticipated therapeutic targets.