subsp.encodes multiple pathways for hydrogen peroxide production
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
Summary Severalspecies import glycerol and related molecules as carbon sources, resulting in the release of hydrogen peroxide (HO), which has been suggested as a pathogenicity mechanism. We systematically deleted genes encoding components of the HOpathways insubsp.GM12 to get insight into the role of candidate factors constituting the pathways. As expected, glycerol metabolism in GM12 is associated with the highest HOproduction compared with glycerophosphocholine. The absence of either L-alpha-glycerophosphate oxidase (GlpO) or the glycerol uptake facilitator GlpF, which is the main glycerol importer in GM12, ceased HOproduction. However, our data did not support any role for the presumed glycerol transport system, GtsABC in glycerol- or glycerophosphocholine-dependent HOproduction. Caprine peripheral blood mononuclear cells (PBMCs) did not show increased cytotoxic effects upon incubation with GM12 in the presence of glycerol, which does not support HOto be a primary pathogenicity mechanism in GM12. abs0010 Graphical abstract http://www.w3.org/1999/xlink float portrait ga1.webp undfig1 anchor portrait graphical abs0015 Highlights • GM12 uses glycerol or glycerophosphocholine to produce HO u0010 • Glycerol is imported by the glycerol uptake facilitator GlpF, not GtsABC, in GM12 u0015 • Glycerophosphocholine metabolism is mediated by GlpU and GlpQ in GM12 u0020 • The multiple HOpathways in GM12 seem to have a minor role in pathogenicity u0025 simple ulist0010 author-highlight
Abstract
Summary Severalspecies import glycerol and related molecules as carbon sources, resulting in the release of hydrogen peroxide (HO), which has been suggested as a pathogenicity mechanism. We systematically deleted genes encoding components of the HOpathways insubsp.GM12 to get insight into the role of candidate factors constituting the pathways. As expected, glycerol metabolism in GM12 is associated with the highest HOproduction compared with glycerophosphocholine. The absence of either L-alpha-glycerophosphate oxidase (GlpO) or the glycerol uptake facilitator GlpF, which is the main glycerol importer in GM12, ceased HOproduction. However, our data did not support any role for the presumed glycerol transport system, GtsABC in glycerol- or glycerophosphocholine-dependent HOproduction. Caprine peripheral blood mononuclear cells (PBMCs) did not show increased cytotoxic effects upon incubation with GM12 in the presence of glycerol, which does not support HOto be a primary pathogenicity mechanism in GM12. abs0010 Graphical abstract http://www.w3.org/1999/xlink float portrait ga1.webp undfig1 anchor portrait graphical abs0015 Highlights • GM12 uses glycerol or glycerophosphocholine to produce HO u0010 • Glycerol is imported by the glycerol uptake facilitator GlpF, not GtsABC, in GM12 u0015 • Glycerophosphocholine metabolism is mediated by GlpU and GlpQ in GM12 u0020 • The multiple HOpathways in GM12 seem to have a minor role in pathogenicity u0025 simple ulist0010 author-highlights abs0020 Microbiology; Systems biology teaser abs0025