@misc{HertelGibhardtMartienssenetal., author = {Hertel, Robert and Gibhardt, Johannes and Martienssen, Marion and Kuhn, Ramona and Commichau, Fabian M.}, title = {Molecular mechanisms underlying glyphosate resistance in bacteria}, series = {Environmental Microbiology}, volume = {23}, journal = {Environmental Microbiology}, number = {6}, issn = {1462-2920}, doi = {10.1111/1462-2920.15534}, pages = {2891 -- 2905}, abstract = {Glyphosate is a nonselective herbicide that kills weeds and other plants competing with crops. Glyphosate specifically inhibits the 5-enolpyruvyl-shikimate-3-phosphate (EPSP) synthase, thereby depleting the cell of EPSP serving as a precursor for biosynthesis of aromatic amino acids. Glyphosate is considered to be toxicologically safe for animals and humans. Therefore, it became the most-important herbicide in agriculture. However, its intensive application in agriculture is a serious environmental issue because it may negatively affect the biodiversity. A few years after the discovery of the mode of action of glyphosate, it has been observed that bacteria evolve glyphosate resistance by acquiring mutations in the EPSP synthase gene, rendering the encoded enzyme less sensitive to the herbicide. The identification of glyphosate-resistant EPSP synthase variants paved the way for engineering crops tolerating increased amounts of the herbicide. This review intends to summarize the molecular mechanisms underlying glyphosate resistance in bacteria. Bacteria can evolve glyphosate resistance by (i) reducing glyphosate sensitivity or elevating production of the EPSP synthase, by (ii) degrading or (iii) detoxifying glyphosate and by (iv) decreasing the uptake or increasing the export of the herbicide. The variety of glyphosate resistance mechanisms illustrates the adaptability of bacteria to anthropogenic substances due to genomic alterations.}, language = {en} } @misc{FrostWeissHerteletal., author = {Frost, Fabian and Weiss, Stefan and Hertel, Johannes and R{\"u}hlemann, Malte and Bang, Corinna and Franke, Andre and Nauck, Matthias and D{\"o}rr, Marcus and V{\"o}lzke, Henry and Roggenbuck, Dirk and Schierack, Peter and V{\"o}lker, Uwe and Homuth, Georg and Aghdassi, Ali A. and Sendler, Matthias and Lerch, Markus M. and Weiss, Frank U.}, title = {Fecal glycoprotein 2 is a marker of gut microbiota dysbiosis and systemic inflammation}, series = {Gut Pathogens}, volume = {16}, journal = {Gut Pathogens}, number = {1}, publisher = {Springer Science and Business Media LLC}, issn = {1757-4749}, doi = {10.1186/s13099-024-00657-1}, pages = {1 -- 11}, abstract = {Background autoantigenic glycoprotein 2 (GP2) is an important component of the innate immune system which originates from the exocrine pancreas as well as from the small intestines. The relationship of GP2 with the intestinal microbiome as well as the systemic implications of increased fecal GP2 levels are, however, still unclear. Therefore, fecal samples from 2,812 individuals of the Study of Health in Pomerania (SHIP) were collected to determine GP2 levels (enzyme-linked immunosorbent assay) and gut microbiota profiles (16 S rRNA gene sequencing). These data were correlated and associated with highly standardised and comprehensive phenotypic data of the study participants. Results Fecal GP2 levels were increased in individuals with higher body mass index and smokers, whereas lower levels were found in case of preserved exocrine pancreatic function, female sex or a healthier diet. Moreover, higher GP2 levels were associated with increased serum levels of high-sensitivity C-reactive protein, loss of gut microbial diversity and an increase of potentially detrimental bacteria (Streptococcus, Haemophilus, Clostridium XIVa, or Collinsella). At the same time, predicted microbial pathways for the biosynthesis of beneficial short-chain fatty acids or lactic acid were depleted in individuals with high fecal GP2. Of note, GP2 exhibited a stronger association to overall microbiome variation than calprotectin. Conclusion Fecal GP2 is a biomarker of gut microbiota dysbiosis and associated with increased systemic inflammation. The intestines may be more important as origin for GP2 than pancreatic acinar cells. Future studies need to investigate the potential clinical value in disease specific patient cohorts.}, language = {en} }