A Mendelian Locus on Chromosome 16 Determines Susceptibility to Doxorubicin Nephropathy in the Mouse
The development of kidney disease is influenced by both genetic and environmental factors. Searching for models of glomerulopathy that display strong gene-environment interaction, we examined the determinants of anthracycline-induced nephropathy, a classic, strain-dependent experimental model applie...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2005-02, Vol.102 (7), p.2502-2507 |
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| creator | Zheng, Zongyu Schmidt-Ott, Kai M. Chua, Streamson Foster, Kirk A. Frankel, Rachelle Z. Pavlidis, Paul Barasch, Jonathan Vivette D. D' Agati Gharavi, Ali G. Lifton, Richard P. |
| description | The development of kidney disease is influenced by both genetic and environmental factors. Searching for models of glomerulopathy that display strong gene-environment interaction, we examined the determinants of anthracycline-induced nephropathy, a classic, strain-dependent experimental model applied to rodents in the past four decades. We produced three crosses derived from mice with contrasting susceptibility to doxorubicin (DOX) nephropathy and, surprisingly, we found that this widely studied model segregates as a single-gene defect with recessive inheritance. By genome-wide analysis of linkage, we mapped the trait locus to chromosome 16A1-B1 (DOXNPH locus) in all three crosses [peak logarithm of odds (lod) score of 92.7, P=1× 10-65]; this interval represents a susceptibility locus for nephropathy. Gene expression analysis indicated that susceptibility alleles at the DOXNPH locus are associated with blunted expression of protein arginine methyltransferase 7 (Prmt7) on chromosome 8, a protein previously implicated in cellular sensitivity to chemotherapeutic agents (lod = 12.4, P = 0.0001). Therefore, Prmt7 expression serves as a molecular marker for susceptibility to DOX nephropathy. Finally, increased variation in the severity of kidney disease among affected mice motivated a second genome-wide search, identifying a locus on chromosome 9 that influences the severity and progression of nephropathy (DOXmod, peak lod score 4.3, P = 0.0018). These data provide genetic and molecular characterization of a previously unrecognized Mendelian trait. Elucidation of DOX nephropathy may simultaneously provide insight into the pathogenesis of renal failure and mechanisms of cytotoxicity induced by chemotherapeutic agents. |
| doi_str_mv | 10.1073/pnas.0409786102 |
| format | Article |
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D' Agati ; Gharavi, Ali G. ; Lifton, Richard P.</creator><creatorcontrib>Zheng, Zongyu ; Schmidt-Ott, Kai M. ; Chua, Streamson ; Foster, Kirk A. ; Frankel, Rachelle Z. ; Pavlidis, Paul ; Barasch, Jonathan ; Vivette D. D' Agati ; Gharavi, Ali G. ; Lifton, Richard P.</creatorcontrib><description>The development of kidney disease is influenced by both genetic and environmental factors. Searching for models of glomerulopathy that display strong gene-environment interaction, we examined the determinants of anthracycline-induced nephropathy, a classic, strain-dependent experimental model applied to rodents in the past four decades. We produced three crosses derived from mice with contrasting susceptibility to doxorubicin (DOX) nephropathy and, surprisingly, we found that this widely studied model segregates as a single-gene defect with recessive inheritance. By genome-wide analysis of linkage, we mapped the trait locus to chromosome 16A1-B1 (DOXNPH locus) in all three crosses [peak logarithm of odds (lod) score of 92.7, P=1× 10-65]; this interval represents a susceptibility locus for nephropathy. Gene expression analysis indicated that susceptibility alleles at the DOXNPH locus are associated with blunted expression of protein arginine methyltransferase 7 (Prmt7) on chromosome 8, a protein previously implicated in cellular sensitivity to chemotherapeutic agents (lod = 12.4, P = 0.0001). Therefore, Prmt7 expression serves as a molecular marker for susceptibility to DOX nephropathy. Finally, increased variation in the severity of kidney disease among affected mice motivated a second genome-wide search, identifying a locus on chromosome 9 that influences the severity and progression of nephropathy (DOXmod, peak lod score 4.3, P = 0.0018). These data provide genetic and molecular characterization of a previously unrecognized Mendelian trait. Elucidation of DOX nephropathy may simultaneously provide insight into the pathogenesis of renal failure and mechanisms of cytotoxicity induced by chemotherapeutic agents.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0409786102</identifier><identifier>PMID: 15699352</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Alleles ; Animals ; Antibiotics, Antineoplastic - toxicity ; Base Sequence ; Biological Sciences ; Chromosome Mapping ; Chromosomes ; Cytotoxicity ; DNA - genetics ; Doxorubicin - toxicity ; Environmental factors ; Female ; Genetic loci ; Genomics ; Genotype-environment interactions ; Histology ; In Situ Hybridization ; Inbreeding ; Kidney diseases ; Kidney Diseases - chemically induced ; Kidney Diseases - genetics ; Kidney Diseases - pathology ; Kidneys ; Lod score ; Male ; Medical genetics ; Medical research ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Oligonucleotide Array Sequence Analysis ; Phenotypes ; Phenotypic traits ; Protein-Arginine N-Methyltransferases - genetics ; Proteins ; Proteinuria ; Rodents</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2005-02, Vol.102 (7), p.2502-2507</ispartof><rights>Copyright 1993/2005 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Feb 15, 2005</rights><rights>Copyright © 2005, The National Academy of Sciences 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-929d933436491838f6cd92c1194155cb587cdb3b517c8d6f6ca9ec7fd8f55e853</citedby><cites>FETCH-LOGICAL-c590t-929d933436491838f6cd92c1194155cb587cdb3b517c8d6f6ca9ec7fd8f55e853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/102/7.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3374645$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3374645$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15699352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Zongyu</creatorcontrib><creatorcontrib>Schmidt-Ott, Kai M.</creatorcontrib><creatorcontrib>Chua, Streamson</creatorcontrib><creatorcontrib>Foster, Kirk A.</creatorcontrib><creatorcontrib>Frankel, Rachelle Z.</creatorcontrib><creatorcontrib>Pavlidis, Paul</creatorcontrib><creatorcontrib>Barasch, Jonathan</creatorcontrib><creatorcontrib>Vivette D. D' Agati</creatorcontrib><creatorcontrib>Gharavi, Ali G.</creatorcontrib><creatorcontrib>Lifton, Richard P.</creatorcontrib><title>A Mendelian Locus on Chromosome 16 Determines Susceptibility to Doxorubicin Nephropathy in the Mouse</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The development of kidney disease is influenced by both genetic and environmental factors. Searching for models of glomerulopathy that display strong gene-environment interaction, we examined the determinants of anthracycline-induced nephropathy, a classic, strain-dependent experimental model applied to rodents in the past four decades. We produced three crosses derived from mice with contrasting susceptibility to doxorubicin (DOX) nephropathy and, surprisingly, we found that this widely studied model segregates as a single-gene defect with recessive inheritance. By genome-wide analysis of linkage, we mapped the trait locus to chromosome 16A1-B1 (DOXNPH locus) in all three crosses [peak logarithm of odds (lod) score of 92.7, P=1× 10-65]; this interval represents a susceptibility locus for nephropathy. Gene expression analysis indicated that susceptibility alleles at the DOXNPH locus are associated with blunted expression of protein arginine methyltransferase 7 (Prmt7) on chromosome 8, a protein previously implicated in cellular sensitivity to chemotherapeutic agents (lod = 12.4, P = 0.0001). Therefore, Prmt7 expression serves as a molecular marker for susceptibility to DOX nephropathy. Finally, increased variation in the severity of kidney disease among affected mice motivated a second genome-wide search, identifying a locus on chromosome 9 that influences the severity and progression of nephropathy (DOXmod, peak lod score 4.3, P = 0.0018). These data provide genetic and molecular characterization of a previously unrecognized Mendelian trait. Elucidation of DOX nephropathy may simultaneously provide insight into the pathogenesis of renal failure and mechanisms of cytotoxicity induced by chemotherapeutic agents.</description><subject>Alleles</subject><subject>Animals</subject><subject>Antibiotics, Antineoplastic - toxicity</subject><subject>Base Sequence</subject><subject>Biological Sciences</subject><subject>Chromosome Mapping</subject><subject>Chromosomes</subject><subject>Cytotoxicity</subject><subject>DNA - genetics</subject><subject>Doxorubicin - toxicity</subject><subject>Environmental factors</subject><subject>Female</subject><subject>Genetic loci</subject><subject>Genomics</subject><subject>Genotype-environment interactions</subject><subject>Histology</subject><subject>In Situ Hybridization</subject><subject>Inbreeding</subject><subject>Kidney diseases</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - genetics</subject><subject>Kidney Diseases - pathology</subject><subject>Kidneys</subject><subject>Lod score</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Phenotypes</subject><subject>Phenotypic traits</subject><subject>Protein-Arginine N-Methyltransferases - genetics</subject><subject>Proteins</subject><subject>Proteinuria</subject><subject>Rodents</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkUtvEzEUhS0EoqGwZoOQxQJWaf0Yj-0FiyrlJaWwANbWjOcOcTRjT20Pav49jhI1BbGyrPud63N8EHpJyQUlkl9OvkkXpCJaqpoS9ggtKNF0WVeaPEYLQphcqopVZ-hZSltCiBaKPEVnVNRac8EWqLvCN-A7GFzj8TrYOeHg8WoTwxhSGAHTGl9Dhjg6Dwl_n5OFKbvWDS7vcA74OtyFOLfOOo-_wlSEU5M3O1yueQP4JswJnqMnfTMkeHE8z9HPjx9-rD4v198-fVldrZdWaJKXmulOc17xYp8qrvradppZSnVFhbCtUNJ2LW8FlVZ1dRk3GqzsO9ULAUrwc_T-sHea2xE6Cz7HZjBTdGMTdyY0zvw98W5jfoXfRpT_Yqzo3x71MdzOkLIZXck7DI2HksNQqUjF6B588w-4DXP0JZthhHLJBFEFujxANoaUIvT3Rigx-_bMvj1zaq8oXj_0f-KPdRXg3RHYK0_rmJGmvMlMPw9Dhrv8YNX_yQK8OgDblEO8JziXVV0J_gf4Kbf5</recordid><startdate>20050215</startdate><enddate>20050215</enddate><creator>Zheng, Zongyu</creator><creator>Schmidt-Ott, Kai M.</creator><creator>Chua, Streamson</creator><creator>Foster, Kirk A.</creator><creator>Frankel, Rachelle Z.</creator><creator>Pavlidis, Paul</creator><creator>Barasch, Jonathan</creator><creator>Vivette D. D' Agati</creator><creator>Gharavi, Ali G.</creator><creator>Lifton, Richard P.</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</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>5PM</scope></search><sort><creationdate>20050215</creationdate><title>A Mendelian Locus on Chromosome 16 Determines Susceptibility to Doxorubicin Nephropathy in the Mouse</title><author>Zheng, Zongyu ; Schmidt-Ott, Kai M. ; Chua, Streamson ; Foster, Kirk A. ; Frankel, Rachelle Z. ; Pavlidis, Paul ; Barasch, Jonathan ; Vivette D. 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D' Agati</au><au>Gharavi, Ali G.</au><au>Lifton, Richard P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Mendelian Locus on Chromosome 16 Determines Susceptibility to Doxorubicin Nephropathy in the Mouse</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2005-02-15</date><risdate>2005</risdate><volume>102</volume><issue>7</issue><spage>2502</spage><epage>2507</epage><pages>2502-2507</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>The development of kidney disease is influenced by both genetic and environmental factors. Searching for models of glomerulopathy that display strong gene-environment interaction, we examined the determinants of anthracycline-induced nephropathy, a classic, strain-dependent experimental model applied to rodents in the past four decades. We produced three crosses derived from mice with contrasting susceptibility to doxorubicin (DOX) nephropathy and, surprisingly, we found that this widely studied model segregates as a single-gene defect with recessive inheritance. By genome-wide analysis of linkage, we mapped the trait locus to chromosome 16A1-B1 (DOXNPH locus) in all three crosses [peak logarithm of odds (lod) score of 92.7, P=1× 10-65]; this interval represents a susceptibility locus for nephropathy. Gene expression analysis indicated that susceptibility alleles at the DOXNPH locus are associated with blunted expression of protein arginine methyltransferase 7 (Prmt7) on chromosome 8, a protein previously implicated in cellular sensitivity to chemotherapeutic agents (lod = 12.4, P = 0.0001). Therefore, Prmt7 expression serves as a molecular marker for susceptibility to DOX nephropathy. Finally, increased variation in the severity of kidney disease among affected mice motivated a second genome-wide search, identifying a locus on chromosome 9 that influences the severity and progression of nephropathy (DOXmod, peak lod score 4.3, P = 0.0018). These data provide genetic and molecular characterization of a previously unrecognized Mendelian trait. Elucidation of DOX nephropathy may simultaneously provide insight into the pathogenesis of renal failure and mechanisms of cytotoxicity induced by chemotherapeutic agents.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>15699352</pmid><doi>10.1073/pnas.0409786102</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alleles Animals Antibiotics, Antineoplastic - toxicity Base Sequence Biological Sciences Chromosome Mapping Chromosomes Cytotoxicity DNA - genetics Doxorubicin - toxicity Environmental factors Female Genetic loci Genomics Genotype-environment interactions Histology In Situ Hybridization Inbreeding Kidney diseases Kidney Diseases - chemically induced Kidney Diseases - genetics Kidney Diseases - pathology Kidneys Lod score Male Medical genetics Medical research Mice Mice, Inbred BALB C Mice, Inbred C57BL Oligonucleotide Array Sequence Analysis Phenotypes Phenotypic traits Protein-Arginine N-Methyltransferases - genetics Proteins Proteinuria Rodents |
| title | A Mendelian Locus on Chromosome 16 Determines Susceptibility to Doxorubicin Nephropathy in the Mouse |
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