Targeted Disruption of Mouse EGF Receptor: Effect of Genetic Background on Mutant Phenotype
Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozy...
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Veröffentlicht in: | Science (American Association for the Advancement of Science) 1995-07, Vol.269 (5221), p.230-234 |
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creator | Threadgill, David W. Dlugosz, Andrzej A. Hansen, Laura A. Tennenbaum, Tamar Lichti, Ulrike Yee, Della LaMantia, Christian Mourton, Tracy Herrup, Karl Harris, Raymond C. Barnard, John A. Yuspa, Stuart H. Coffey, Robert J. Magnuson, Terry |
description | Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities. |
doi_str_mv | 10.1126/science.7618084 |
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The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.7618084</identifier><identifier>PMID: 7618084</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Abnormalities, Multiple - genetics ; Alleles ; Animals ; Base Sequence ; Biological and medical sciences ; Brain - abnormalities ; Brain - cytology ; Cell Division ; Cellular biology ; Classical genetics, quantitative genetics, hybrids ; Digestive System - cytology ; Digestive System Abnormalities ; Embryo implantation ; Embryonic and Fetal Development ; Embryos ; ErbB Receptors - deficiency ; ErbB Receptors - genetics ; ErbB Receptors - physiology ; Exons ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Targeting ; Genetics ; Genetics of eukaryotes. Biological and molecular evolution ; Giant cells ; Hair - abnormalities ; Hepatocytes ; Histology ; Homozygote ; Individualized Instruction ; Kidney - cytology ; Kidney cells ; Lung - cytology ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Phenotype ; Phenotypes ; Pregnancy ; Rodents ; Scientific Concepts ; Skin - cytology ; Skin Abnormalities ; Vertebrata</subject><ispartof>Science (American Association for the Advancement of Science), 1995-07, Vol.269 (5221), p.230-234</ispartof><rights>Copyright 1995 American Association for the Advancement of Science</rights><rights>1995 INIST-CNRS</rights><rights>Copyright American Association for the Advancement of Science Jul 14, 1995</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-5b2eb5fe9ee9ca50e98e7dff416138bf2afbc07b3e9e9d8e19d33675a4da6e1a3</citedby><cites>FETCH-LOGICAL-c528t-5b2eb5fe9ee9ca50e98e7dff416138bf2afbc07b3e9e9d8e19d33675a4da6e1a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2888447$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2888447$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,803,2884,2885,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3583234$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7618084$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Threadgill, David W.</creatorcontrib><creatorcontrib>Dlugosz, Andrzej A.</creatorcontrib><creatorcontrib>Hansen, Laura A.</creatorcontrib><creatorcontrib>Tennenbaum, Tamar</creatorcontrib><creatorcontrib>Lichti, Ulrike</creatorcontrib><creatorcontrib>Yee, Della</creatorcontrib><creatorcontrib>LaMantia, Christian</creatorcontrib><creatorcontrib>Mourton, Tracy</creatorcontrib><creatorcontrib>Herrup, Karl</creatorcontrib><creatorcontrib>Harris, Raymond C.</creatorcontrib><creatorcontrib>Barnard, John A.</creatorcontrib><creatorcontrib>Yuspa, Stuart H.</creatorcontrib><creatorcontrib>Coffey, Robert J.</creatorcontrib><creatorcontrib>Magnuson, Terry</creatorcontrib><title>Targeted Disruption of Mouse EGF Receptor: Effect of Genetic Background on Mutant Phenotype</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.</description><subject>Abnormalities, Multiple - genetics</subject><subject>Alleles</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Brain - abnormalities</subject><subject>Brain - cytology</subject><subject>Cell Division</subject><subject>Cellular biology</subject><subject>Classical genetics, quantitative genetics, hybrids</subject><subject>Digestive System - cytology</subject><subject>Digestive System Abnormalities</subject><subject>Embryo implantation</subject><subject>Embryonic and Fetal Development</subject><subject>Embryos</subject><subject>ErbB Receptors - deficiency</subject><subject>ErbB Receptors - genetics</subject><subject>ErbB Receptors - physiology</subject><subject>Exons</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Targeting</subject><subject>Genetics</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Giant cells</subject><subject>Hair - abnormalities</subject><subject>Hepatocytes</subject><subject>Histology</subject><subject>Homozygote</subject><subject>Individualized Instruction</subject><subject>Kidney - cytology</subject><subject>Kidney cells</subject><subject>Lung - cytology</subject><subject>Male</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Pregnancy</subject><subject>Rodents</subject><subject>Scientific Concepts</subject><subject>Skin - cytology</subject><subject>Skin Abnormalities</subject><subject>Vertebrata</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0b9v1DAUB3ALgcpRmFlAshCCKa0dx7-6QbkeSK1aoTIxRI7zXHLc2cF2hv73-HTRIXWgk4fv5z3r6YvQa0pOKK3FabIDeAsnUlBFVPMELSjRvNI1YU_RghAmKkUkf45epLQmpGSaHaGjmS_Qz1sT7yBDj78MKU5jHoLHweGrMCXAy9UF_g4WxhziGV46Bzbv0hV4yIPFn439fRfD5Htcxq6mbHzGN7_Ah3w_wkv0zJlNglfze4x-XCxvz79Wl9erb-efLivLa5Ur3tXQcQcaQFvDCWgFsneuoYIy1bnauM4S2bEidK-A6p4xIblpeiOAGnaMPuz3jjH8mSDldjskC5uN8VDOaKVsiGCaFPjx_7BhnHGqmkdXUiE1kZoX-O4BXIcp-nJuW1PGleBEF3S6RzaGlCK4dozD1sT7lpJ2V2M719jOvZSJt_PaqdtCf_D_8vdzbpI1GxeNt0M6sPIxq9mOvdmzdSoNHuJaKdU0kv0FV9CviQ</recordid><startdate>19950714</startdate><enddate>19950714</enddate><creator>Threadgill, David W.</creator><creator>Dlugosz, Andrzej A.</creator><creator>Hansen, Laura A.</creator><creator>Tennenbaum, Tamar</creator><creator>Lichti, Ulrike</creator><creator>Yee, Della</creator><creator>LaMantia, Christian</creator><creator>Mourton, Tracy</creator><creator>Herrup, Karl</creator><creator>Harris, Raymond C.</creator><creator>Barnard, John A.</creator><creator>Yuspa, Stuart H.</creator><creator>Coffey, Robert J.</creator><creator>Magnuson, Terry</creator><general>American Society for the Advancement of Science</general><general>American Association for the Advancement of Science</general><general>The American Association for the Advancement of Science</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>0-V</scope><scope>3V.</scope><scope>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88B</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8BQ</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CJNVE</scope><scope>D1I</scope><scope>DWQXO</scope><scope>F28</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>HCIFZ</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9-</scope><scope>K9.</scope><scope>KB.</scope><scope>KR7</scope><scope>L6V</scope><scope>L7M</scope><scope>LK8</scope><scope>L~C</scope><scope>L~D</scope><scope>M0K</scope><scope>M0P</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>MBDVC</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PCBAR</scope><scope>PDBOC</scope><scope>PQEDU</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>R05</scope><scope>RC3</scope><scope>7TO</scope><scope>7X8</scope></search><sort><creationdate>19950714</creationdate><title>Targeted Disruption of Mouse EGF Receptor: Effect of Genetic Background on Mutant Phenotype</title><author>Threadgill, David W. ; Dlugosz, Andrzej A. ; Hansen, Laura A. ; Tennenbaum, Tamar ; Lichti, Ulrike ; Yee, Della ; LaMantia, Christian ; Mourton, Tracy ; Herrup, Karl ; Harris, Raymond C. ; Barnard, John A. ; Yuspa, Stuart H. ; Coffey, Robert J. ; Magnuson, Terry</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-5b2eb5fe9ee9ca50e98e7dff416138bf2afbc07b3e9e9d8e19d33675a4da6e1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Abnormalities, Multiple - genetics</topic><topic>Alleles</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Brain - abnormalities</topic><topic>Brain - cytology</topic><topic>Cell Division</topic><topic>Cellular biology</topic><topic>Classical genetics, quantitative genetics, hybrids</topic><topic>Digestive System - cytology</topic><topic>Digestive System Abnormalities</topic><topic>Embryo implantation</topic><topic>Embryonic and Fetal Development</topic><topic>Embryos</topic><topic>ErbB Receptors - deficiency</topic><topic>ErbB Receptors - genetics</topic><topic>ErbB Receptors - physiology</topic><topic>Exons</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Targeting</topic><topic>Genetics</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>Giant cells</topic><topic>Hair - abnormalities</topic><topic>Hepatocytes</topic><topic>Histology</topic><topic>Homozygote</topic><topic>Individualized Instruction</topic><topic>Kidney - cytology</topic><topic>Kidney cells</topic><topic>Lung - cytology</topic><topic>Male</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Pregnancy</topic><topic>Rodents</topic><topic>Scientific Concepts</topic><topic>Skin - cytology</topic><topic>Skin Abnormalities</topic><topic>Vertebrata</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Threadgill, David W.</creatorcontrib><creatorcontrib>Dlugosz, Andrzej A.</creatorcontrib><creatorcontrib>Hansen, Laura A.</creatorcontrib><creatorcontrib>Tennenbaum, Tamar</creatorcontrib><creatorcontrib>Lichti, Ulrike</creatorcontrib><creatorcontrib>Yee, 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The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>7618084</pmid><doi>10.1126/science.7618084</doi><tpages>5</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0036-8075 |
ispartof | Science (American Association for the Advancement of Science), 1995-07, Vol.269 (5221), p.230-234 |
issn | 0036-8075 1095-9203 |
language | eng |
recordid | cdi_proquest_miscellaneous_77406390 |
source | MEDLINE; JSTOR Archive Collection A-Z Listing; American Association for the Advancement of Science |
subjects | Abnormalities, Multiple - genetics Alleles Animals Base Sequence Biological and medical sciences Brain - abnormalities Brain - cytology Cell Division Cellular biology Classical genetics, quantitative genetics, hybrids Digestive System - cytology Digestive System Abnormalities Embryo implantation Embryonic and Fetal Development Embryos ErbB Receptors - deficiency ErbB Receptors - genetics ErbB Receptors - physiology Exons Female Fundamental and applied biological sciences. Psychology Gene Targeting Genetics Genetics of eukaryotes. Biological and molecular evolution Giant cells Hair - abnormalities Hepatocytes Histology Homozygote Individualized Instruction Kidney - cytology Kidney cells Lung - cytology Male Mice Molecular Sequence Data Mutation Phenotype Phenotypes Pregnancy Rodents Scientific Concepts Skin - cytology Skin Abnormalities Vertebrata |
title | Targeted Disruption of Mouse EGF Receptor: Effect of Genetic Background on Mutant Phenotype |
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