Genetic and epigenetic control of the efficiency and fidelity of cross‐species prion transmission
Summary Self‐perpetuating amyloid‐based protein isoforms (prions) transmit neurodegenerative diseases in mammals and phenotypic traits in yeast. Although mechanisms that control species specificity of prion transmission are poorly understood, studies of closely related orthologues of yeast prion pro...
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| Veröffentlicht in: | Molecular microbiology 2010-06, Vol.76 (6), p.1483-1499 |
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| creator | Chen, Buxin Bruce, Kathryn L. Newnam, Gary P. Gyoneva, Stefka Romanyuk, Andrey V. Chernoff, Yury O. |
| description | Summary
Self‐perpetuating amyloid‐based protein isoforms (prions) transmit neurodegenerative diseases in mammals and phenotypic traits in yeast. Although mechanisms that control species specificity of prion transmission are poorly understood, studies of closely related orthologues of yeast prion protein Sup35 demonstrate that cross‐species prion transmission is modulated by both genetic (specific sequence elements) and epigenetic (prion variants, or ‘strains’) factors. Depending on the prion variant, the species barrier could be controlled at the level of either heterologous co‐aggregation or conversion of the aggregate‐associated heterologous protein into a prion polymer. Sequence divergence influences cross‐species transmission of different prion variants in opposing ways. The ability of a heterologous prion domain to either faithfully reproduce or irreversibly switch the variant‐specific prion patterns depends on both sequence divergence and the prion variant. Sequence variations within different modules of prion domains contribute to transmission barriers in different cross‐species combinations. Individual amino acid substitutions within short amyloidogenic stretches drastically alter patterns of cross‐species prion conversion, implicating these stretches as major determinants of species specificity. |
| doi_str_mv | 10.1111/j.1365-2958.2010.07177.x |
| format | Article |
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Self‐perpetuating amyloid‐based protein isoforms (prions) transmit neurodegenerative diseases in mammals and phenotypic traits in yeast. Although mechanisms that control species specificity of prion transmission are poorly understood, studies of closely related orthologues of yeast prion protein Sup35 demonstrate that cross‐species prion transmission is modulated by both genetic (specific sequence elements) and epigenetic (prion variants, or ‘strains’) factors. Depending on the prion variant, the species barrier could be controlled at the level of either heterologous co‐aggregation or conversion of the aggregate‐associated heterologous protein into a prion polymer. Sequence divergence influences cross‐species transmission of different prion variants in opposing ways. The ability of a heterologous prion domain to either faithfully reproduce or irreversibly switch the variant‐specific prion patterns depends on both sequence divergence and the prion variant. Sequence variations within different modules of prion domains contribute to transmission barriers in different cross‐species combinations. Individual amino acid substitutions within short amyloidogenic stretches drastically alter patterns of cross‐species prion conversion, implicating these stretches as major determinants of species specificity.</description><identifier>ISSN: 0950-382X</identifier><identifier>EISSN: 1365-2958</identifier><identifier>DOI: 10.1111/j.1365-2958.2010.07177.x</identifier><identifier>PMID: 20444092</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Amino Acid Sequence ; Amino acids ; Amyloid - metabolism ; Bacteria ; Bacterial proteins ; Biological and medical sciences ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Epigenetics ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation, Fungal ; Gene Transfer, Horizontal ; Genotype & phenotype ; Mammals ; Medical sciences ; Microbiology ; Molecular Sequence Data ; Neurology ; Non conventional transmissible agents ; Peptide Termination Factors - genetics ; Peptide Termination Factors - metabolism ; Polymorphism, Genetic ; Prions ; Saccharomyces cerevisiae - genetics ; Saccharomyces cerevisiae - metabolism ; Saccharomyces cerevisiae Proteins - genetics ; Saccharomyces cerevisiae Proteins - metabolism ; Sequence Alignment</subject><ispartof>Molecular microbiology, 2010-06, Vol.76 (6), p.1483-1499</ispartof><rights>2010 Blackwell Publishing Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Ltd. Jun 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6287-66466977d61dbe0f6054b0bf782f3a92e136fb77941662b854069eb1c5a0e6fa3</citedby><cites>FETCH-LOGICAL-c6287-66466977d61dbe0f6054b0bf782f3a92e136fb77941662b854069eb1c5a0e6fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2958.2010.07177.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2958.2010.07177.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,1433,27923,27924,45573,45574,46408,46832</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22862217$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20444092$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Buxin</creatorcontrib><creatorcontrib>Bruce, Kathryn L.</creatorcontrib><creatorcontrib>Newnam, Gary P.</creatorcontrib><creatorcontrib>Gyoneva, Stefka</creatorcontrib><creatorcontrib>Romanyuk, Andrey V.</creatorcontrib><creatorcontrib>Chernoff, Yury O.</creatorcontrib><title>Genetic and epigenetic control of the efficiency and fidelity of cross‐species prion transmission</title><title>Molecular microbiology</title><addtitle>Mol Microbiol</addtitle><description>Summary
Self‐perpetuating amyloid‐based protein isoforms (prions) transmit neurodegenerative diseases in mammals and phenotypic traits in yeast. Although mechanisms that control species specificity of prion transmission are poorly understood, studies of closely related orthologues of yeast prion protein Sup35 demonstrate that cross‐species prion transmission is modulated by both genetic (specific sequence elements) and epigenetic (prion variants, or ‘strains’) factors. Depending on the prion variant, the species barrier could be controlled at the level of either heterologous co‐aggregation or conversion of the aggregate‐associated heterologous protein into a prion polymer. Sequence divergence influences cross‐species transmission of different prion variants in opposing ways. The ability of a heterologous prion domain to either faithfully reproduce or irreversibly switch the variant‐specific prion patterns depends on both sequence divergence and the prion variant. Sequence variations within different modules of prion domains contribute to transmission barriers in different cross‐species combinations. Individual amino acid substitutions within short amyloidogenic stretches drastically alter patterns of cross‐species prion conversion, implicating these stretches as major determinants of species specificity.</description><subject>Amino Acid Sequence</subject><subject>Amino acids</subject><subject>Amyloid - metabolism</subject><subject>Bacteria</subject><subject>Bacterial proteins</subject><subject>Biological and medical sciences</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Epigenetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation, Fungal</subject><subject>Gene Transfer, Horizontal</subject><subject>Genotype & phenotype</subject><subject>Mammals</subject><subject>Medical sciences</subject><subject>Microbiology</subject><subject>Molecular Sequence Data</subject><subject>Neurology</subject><subject>Non conventional transmissible agents</subject><subject>Peptide Termination Factors - genetics</subject><subject>Peptide Termination Factors - metabolism</subject><subject>Polymorphism, Genetic</subject><subject>Prions</subject><subject>Saccharomyces cerevisiae - genetics</subject><subject>Saccharomyces cerevisiae - metabolism</subject><subject>Saccharomyces cerevisiae Proteins - genetics</subject><subject>Saccharomyces cerevisiae Proteins - metabolism</subject><subject>Sequence Alignment</subject><issn>0950-382X</issn><issn>1365-2958</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1uEzEQxy0EoqHwCmiFhDht6u-PA0ioglKpVS8gcbO83nHraLMO6w00Nx6BZ-RJ8CZpoFzAF3s8vxnNf_4IVQTPSTknizlhUtTUCD2nuPxiRZSa3z5As0PiIZphI3DNNP18hJ7kvMCYMCzZY3REMeccGzpD_gx6GKOvXN9WsIrX-9CnfhxSV6VQjTdQQQjRR-j9ZguG2EIXx82U9kPK-ef3H3kFhcjVaoipr8bB9XkZcy7BU_QouC7Ds_19jD69f_fx9EN9cXV2fvr2ovaSalVLyaU0SrWStA3gILHgDW6C0jQwZygUaaFRynAiJW204FgaaIgXDoMMjh2jN7u-q3WzhNZDkeA6WwZaumFjk4v2fqaPN_Y6fbUMU6GELg1e7RsM6csa8miLAg9d53pI62wV55Jyxei_ScaMkYaIQr74i1yk9dCXPViBudKEU14gvYO2yxwgHIYm2E6O24WdjLWTsXZy3G4dt7el9Pmfog-FdxYX4OUecNm7LhRjfMy_OaolpUQV7vWO-xY72Pz3APby8nx6sV9h5MjG</recordid><startdate>201006</startdate><enddate>201006</enddate><creator>Chen, Buxin</creator><creator>Bruce, Kathryn L.</creator><creator>Newnam, Gary P.</creator><creator>Gyoneva, Stefka</creator><creator>Romanyuk, Andrey V.</creator><creator>Chernoff, Yury O.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201006</creationdate><title>Genetic and epigenetic control of the efficiency and fidelity of cross‐species prion transmission</title><author>Chen, Buxin ; Bruce, Kathryn L. ; Newnam, Gary P. ; Gyoneva, Stefka ; Romanyuk, Andrey V. ; Chernoff, Yury O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6287-66466977d61dbe0f6054b0bf782f3a92e136fb77941662b854069eb1c5a0e6fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Amino Acid Sequence</topic><topic>Amino acids</topic><topic>Amyloid - metabolism</topic><topic>Bacteria</topic><topic>Bacterial proteins</topic><topic>Biological and medical sciences</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Epigenetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation, Fungal</topic><topic>Gene Transfer, Horizontal</topic><topic>Genotype & phenotype</topic><topic>Mammals</topic><topic>Medical sciences</topic><topic>Microbiology</topic><topic>Molecular Sequence Data</topic><topic>Neurology</topic><topic>Non conventional transmissible agents</topic><topic>Peptide Termination Factors - genetics</topic><topic>Peptide Termination Factors - metabolism</topic><topic>Polymorphism, Genetic</topic><topic>Prions</topic><topic>Saccharomyces cerevisiae - genetics</topic><topic>Saccharomyces cerevisiae - metabolism</topic><topic>Saccharomyces cerevisiae Proteins - genetics</topic><topic>Saccharomyces cerevisiae Proteins - metabolism</topic><topic>Sequence Alignment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Buxin</creatorcontrib><creatorcontrib>Bruce, Kathryn L.</creatorcontrib><creatorcontrib>Newnam, Gary P.</creatorcontrib><creatorcontrib>Gyoneva, Stefka</creatorcontrib><creatorcontrib>Romanyuk, Andrey V.</creatorcontrib><creatorcontrib>Chernoff, Yury O.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Buxin</au><au>Bruce, Kathryn L.</au><au>Newnam, Gary P.</au><au>Gyoneva, Stefka</au><au>Romanyuk, Andrey V.</au><au>Chernoff, Yury O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic and epigenetic control of the efficiency and fidelity of cross‐species prion transmission</atitle><jtitle>Molecular microbiology</jtitle><addtitle>Mol Microbiol</addtitle><date>2010-06</date><risdate>2010</risdate><volume>76</volume><issue>6</issue><spage>1483</spage><epage>1499</epage><pages>1483-1499</pages><issn>0950-382X</issn><eissn>1365-2958</eissn><abstract>Summary
Self‐perpetuating amyloid‐based protein isoforms (prions) transmit neurodegenerative diseases in mammals and phenotypic traits in yeast. Although mechanisms that control species specificity of prion transmission are poorly understood, studies of closely related orthologues of yeast prion protein Sup35 demonstrate that cross‐species prion transmission is modulated by both genetic (specific sequence elements) and epigenetic (prion variants, or ‘strains’) factors. Depending on the prion variant, the species barrier could be controlled at the level of either heterologous co‐aggregation or conversion of the aggregate‐associated heterologous protein into a prion polymer. Sequence divergence influences cross‐species transmission of different prion variants in opposing ways. The ability of a heterologous prion domain to either faithfully reproduce or irreversibly switch the variant‐specific prion patterns depends on both sequence divergence and the prion variant. Sequence variations within different modules of prion domains contribute to transmission barriers in different cross‐species combinations. Individual amino acid substitutions within short amyloidogenic stretches drastically alter patterns of cross‐species prion conversion, implicating these stretches as major determinants of species specificity.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20444092</pmid><doi>10.1111/j.1365-2958.2010.07177.x</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino Acid Sequence Amino acids Amyloid - metabolism Bacteria Bacterial proteins Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Epigenetics Fundamental and applied biological sciences. Psychology Gene Expression Regulation, Fungal Gene Transfer, Horizontal Genotype & phenotype Mammals Medical sciences Microbiology Molecular Sequence Data Neurology Non conventional transmissible agents Peptide Termination Factors - genetics Peptide Termination Factors - metabolism Polymorphism, Genetic Prions Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Sequence Alignment |
| title | Genetic and epigenetic control of the efficiency and fidelity of cross‐species prion transmission |
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