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The eyeless mouse mutation (ey1) removes an alternative start codon from the Rx/rax homeobox gene

dc.contributor.authorTucker, Priscilla K.en_US
dc.contributor.authorLaemle, Loisen_US
dc.contributor.authorMunson, Amandaen_US
dc.contributor.authorKanekar, Shami L.en_US
dc.contributor.authorOliver, Edward R.en_US
dc.contributor.authorBrown, Nadean L.en_US
dc.contributor.authorSchlecht, Hansen_US
dc.contributor.authorVetter, Monica L.en_US
dc.contributor.authorGlaser, Tomen_US
dc.date.accessioned2006-04-19T14:20:03Z
dc.date.available2006-04-19T14:20:03Z
dc.date.issued2001-09en_US
dc.identifier.citationTucker, Priscilla; Laemle, Lois; Munson, Amanda; Kanekar, Shami; Oliver, Edward R.; Brown, Nadean; Schlecht, Hans; Vetter, Monica; Glaser, Tom (2001)."The eyeless mouse mutation (ey1) removes an alternative start codon from the Rx/rax homeobox gene." genesis 31(1): 43-53. <http://hdl.handle.net/2027.42/35266>en_US
dc.identifier.issn1526-954Xen_US
dc.identifier.issn1526-968Xen_US
dc.identifier.urihttps://hdl.handle.net/2027.42/35266
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=11668677&dopt=citationen_US
dc.description.abstractSummary: The eyeless inbred mouse strain ZRDCT has long served as a spontaneous model for human anophthalmia and the evolutionary reduction of eyes that has occurred in some naturally blind mammals. ZRDCT mice have orbits but lack eyes and optic tracts and have hypothalamic abnormalities. Segregation data suggest that a small number of interacting genes are responsible, including at least one major recessive locus, ey1 . Although predicted since the 1940s, these loci were never identified. We mapped ey1 to chromosome 18 using an F2 genome scan and there found a Met10→Leu mutation in Rx/rax , a homeobox gene that is expressed in the anterior headfold, developing retina, pineal, and hypothalamus and is translated via a leaky scanning mechanism. The mutation affects a conserved AUG codon that functions as an alternative translation initiation site and consequently reduces the abundance of Rx protein. In contrast to a targeted Rx null allele, which causes anophthalmia, central nervous system defects, and neonatal death, the hypomorphic M10L allele is fully viable. genesis 31:43–53, 2001. © 2001 Wiley-Liss, Inc.en_US
dc.format.extent499781 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherJohn Wiley & Sons, Inc.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherGeneticsen_US
dc.titleThe eyeless mouse mutation (ey1) removes an alternative start codon from the Rx/rax homeobox geneen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelGeneticsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumMuseum of Zoology and Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumDepartments of Internal Medicine and Human Genetics, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumDepartments of Internal Medicine and Human Genetics, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumDepartments of Internal Medicine and Human Genetics, University of Michigan, Ann Arbor, Michigan ; 4510 MSRB I, Box 0650, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0650en_US
dc.contributor.affiliationotherDepartments of Anatomy, Cell Biology and Molecular Medicine and Ophthalmology, University of Medicine and Dentistry of New Jersey, Newark, New Jerseyen_US
dc.contributor.affiliationotherDepartment of Neurobiology and Anatomy, University of Utah, Salt Lake City, Utahen_US
dc.contributor.affiliationotherChildren's Memorial Institute for Education and Research, Department of Pediatrics, Northwestern University, Chicago, Illinoisen_US
dc.contributor.affiliationotherDepartments of Anatomy, Cell Biology and Molecular Medicine and Ophthalmology, University of Medicine and Dentistry of New Jersey, Newark, New Jerseyen_US
dc.contributor.affiliationotherDepartment of Neurobiology and Anatomy, University of Utah, Salt Lake City, Utahen_US
dc.identifier.pmid11668677en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/35266/1/10003_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/gene.10003en_US
dc.identifier.sourcegenesisen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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