{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Owl":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000-biopax2.owl","https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000-biopax3.owl"],"Svg":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000.svg"],"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000_url.xml","https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000_urn.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000.vcml","https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000.m","https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000.xpp","https://www.ebi.ac.uk/biomodels/model/download/MODEL1710040000?filename=MODEL1710040000.sci"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Vijayalakshmi Chelliah"],"curationStatus":["Non-curated"],"modellingApproach":["constraint-based model"],"levelVersion":["L3V1"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL1710040000"],"publication_pubmed":["29377524"],"isPrivate":["false"],"repository":["BioModels"],"modelFormat":["SBML"],"omics_type":["Models"],"tokenised_name":["Kees2018 Genome scale constraint based model of the mucin degrader Akkermansia muciniphila"],"publication_year":["2018"],"submissionId":["MODEL1710040000"],"publication_authors":["van der Ark KCH, Aalvink S, Suarez-Diez M, Schaap PJ, de Vos WM, Belzer C"],"first_author":["van der Ark KCH"],"publication":["29377524,\n The abundance of the human intestinal symbiont Akkermansia muciniphila has found to be inversely correlated with several diseases, including metabolic syndrome and obesity. A. muciniphila is known to use mucin as sole carbon and nitrogen source. To study the physiology and the potential for therapeutic applications of this bacterium, we designed a defined minimal medium. The composition of the medium was based on the genome-scale metabolic model of A. muciniphila and the composition of mucin. Our results indicate that A. muciniphila does not code for GlmS, the enzyme that mediates the conversion of fructose-6-phosphate (Fru6P) to glucosamine-6-phosphate (GlcN6P), which is essential in peptidoglycan formation. The only annotated enzyme that could mediate this conversion is Amuc-NagB on locus Amuc_1822. We found that Amuc-NagB was unable to form GlcN6P from Fru6P at physiological conditions, while it efficiently catalyzed the reverse reaction. To overcome this inability, N-acetylglucosamine needs to be present in the medium for A. muciniphila growth. With these findings, the genome-scale metabolic model was updated and used to accurately predict growth of A. muciniphila on synthetic media. The finding that A. muciniphila has a necessity for GlcNAc, which is present in mucin further prompts the adaptation to its mucosal niche.. 3, 11.\n Laboratory of Microbiology, Wageningen University & Research, Stippeneng 4, 6708 WE, Wageningen, The Netherlands."],"submitter_mail":["viji@ebi.ac.uk"],"submitter_affiliation":["EMBL-EBI"],"pubmed_abstract":["The abundance of the human intestinal symbiont Akkermansia muciniphila has found to be inversely correlated with several diseases, including metabolic syndrome and obesity. A. muciniphila is known to use mucin as sole carbon and nitrogen source. To study the physiology and the potential for therapeutic applications of this bacterium, we designed a defined minimal medium. The composition of the medium was based on the genome-scale metabolic model of A. muciniphila and the composition of mucin. Our results indicate that A. muciniphila does not code for GlmS, the enzyme that mediates the conversion of fructose-6-phosphate (Fru6P) to glucosamine-6-phosphate (GlcN6P), which is essential in peptidoglycan formation. The only annotated enzyme that could mediate this conversion is Amuc-NagB on locus Amuc_1822. We found that Amuc-NagB was unable to form GlcN6P from Fru6P at physiological conditions, while it efficiently catalyzed the reverse reaction. To overcome this inability, N-acetylglucosamine needs to be present in the medium for A. muciniphila growth. With these findings, the genome-scale metabolic model was updated and used to accurately predict growth of A. muciniphila on synthetic media. The finding that A. muciniphila has a necessity for GlcNAc, which is present in mucin further prompts the adaptation to its mucosal niche."],"pubmed_title":["Model-driven design of a minimal medium for Akkermansia muciniphila confirms mucus adaptation."],"pubmed_authors":["van der Ark Kees C H KCH, Aalvink Steven S, Suarez-Diez Maria M, Schaap Peter J PJ, de Vos Willem M WM, Belzer Clara C"],"name_synonyms":["scale (sensu Metazoa), scale tissue, scales, scale, Genomes, Mucin., plant peltate hair, peltate hair"],"pubmed_abstract_synonyms":["sodium salt, Forms, other disease, scale tissue, human being, 2-amino-2-deoxyglucose, artificial sequence, Dona S, peltate hair, barium salt, postnatal development, obesity disease, X Syndrome, carbon, growth and development, Pi, composed of, Xicil, Glukosamin, Adiposis, Obesity, Obese, Dysmetabolic, Cardiometabolic Syndromes, unspecified, diseases, Metabolic Cardiovascular Syndrome, Carbon-12, Mucin., symptoms, disease or disorder, GlcN, diseases 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- Genome-scale constraint-based model of the mucin-degrader Akkermansia muciniphila","description":"\n \n Kees2018 - Genome-scale constraint-based\n model of the mucin-degrader Akkermansia\n muciniphila\n \n This model is described in the article:\n \n Model-driven design of a\n minimal medium for Akkermansia muciniphila confirms mucus\n adaptation.\n \n van der Ark KCH, Aalvink S,\n Suarez-Diez M, Schaap PJ, de Vos WM, Belzer C.\n Microb Biotechnol 2018 Jan; :\n Abstract:\n \n The abundance of the human intestinal symbiont Akkermansia\n muciniphila has found to be inversely correlated with several\n diseases, including metabolic syndrome and obesity.\n A. muciniphila is known to use mucin as sole carbon and\n nitrogen source. To study the physiology and the potential for\n therapeutic applications of this bacterium, we designed a\n defined minimal medium. The composition of the medium was based\n on the genome-scale metabolic model of A. muciniphila and\n the composition of mucin. Our results indicate that\n A. muciniphila does not code for GlmS, the enzyme that\n mediates the conversion of fructose-6-phosphate (Fru6P) to\n glucosamine-6-phosphate (GlcN6P), which is essential in\n peptidoglycan formation. The only annotated enzyme that could\n mediate this conversion is Amuc-NagB on locus Amuc_1822. We\n found that Amuc-NagB was unable to form GlcN6P from Fru6P at\n physiological conditions, while it efficiently catalyzed the\n reverse reaction. To overcome this inability,\n N-acetylglucosamine needs to be present in the medium for\n A. muciniphila growth. With these findings, the\n genome-scale metabolic model was updated and used to accurately\n predict growth of A. muciniphila on synthetic media. The\n finding that A. muciniphila has a necessity for GlcNAc,\n which is present in mucin further prompts the adaptation to its\n mucosal niche.\n \n \n \n This model is hosted on \n BioModels Database\n and identified by: \n MODEL1710040000.\n To cite BioModels Database, please use: \n Chelliah V et al. BioModels: ten-year\n anniversary. Nucl. Acids Res. 2015, 43(Database\n issue):D542-8.\n \n \n To the extent possible under law, all copyright and related or\n neighbouring rights to this encoded model have been dedicated to\n the public domain worldwide. Please refer to \n CC0\n Public Domain Dedication for more information.\n \n \n ","dates":{"last_modification":"2018-02-02","publication":"2021-02-15","submission":"2017-10-04"},"accession":"MODEL1710040000","cross_references":{"pubmed":["29377524"],"biomodels__db":["MODEL1710040000"]}}