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dc.contributor.authorMastick, Grant S.en_US
dc.contributor.authorFan, Chen-Mingen_US
dc.contributor.authorTessier-Lavigne, Marcen_US
dc.contributor.authorSerbedzija, George N.en_US
dc.contributor.authorMcMahon, Andrew P.en_US
dc.contributor.authorEaster, Stephen S.en_US
dc.date.accessioned2007-04-06T18:24:11Z
dc.date.available2007-04-06T18:24:11Z
dc.date.issued1996-10-14en_US
dc.identifier.citationMastick, Grant S.; Fan, Chen-Ming; Tessier-Lavigne, Marc; Serbedzija, George N.; McMahon, Andrew P.; Easter, Stephen S. (1996)."Early deletion of neuromeres in Wnt-1 -/- mutant mice: Evaluation by morphological and molecular markers." The Journal of Comparative Neurology 374(2): 246-258. <http://hdl.handle.net/2027.42/50070>en_US
dc.identifier.issn0021-9967en_US
dc.identifier.issn1096-9861en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50070
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8906497&dopt=citationen_US
dc.description.abstractThe Wnt-1 gene is required for the development of midbrain and cerebellum; previous work showed that knockout of Wnt-1 causes the loss of most molecular markers of these structures in early embryos and deletion of these structures by birth. However, neither the extent of early neuronal defects nor any possible alterations in structures adjacent to presumptive midbrain and cerebellum were examined. By using a neuron-specific antibody and fluorescent axon tracers, we show that central and peripheral neuronal development are altered in mutants during initial axonogenesis on embryonic day 9.5. The absence of neuronal landmarks, including oculomotor and trochlear nerves and cerebellar plate, suggests that both mesencephalon and rhombomere 1 (r1) are deleted, with the remaining neural tube fused to form a new border between the caudalmost portion of the prosencephalon (prosomere 1, or p1) and r2. Central axons accurately traverse this novel border by forming normal longitudinal tracts into the rhombencephalon, implying that the cues that direct these axons are aligned across neuromeres and are not affected by the deletion. The presence of intact p1 and r2 is further supported by the retention of markers for these two neuromeres, including a marker of p1, the Sim-2 gene, and an r2-specific lacZ transgene in mutant embryos. In addition, alterations in the Sim-2 expression domain in ventral prosencephalon, rostral to p1, provide novel evidence for Wnt-1 function in this region. © 1996 Wiley-Liss, Inc.en_US
dc.format.extent1593059 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherJohn Wiley & Sons, Inc.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleEarly deletion of neuromeres in Wnt-1 -/- mutant mice: Evaluation by morphological and molecular markersen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Biology, University of Michigan, Ann Arbor, Michigan 48109 ; Department of Biology, University of Michigan, Ann Arbor, MI 48109.en_US
dc.contributor.affiliationumDepartment of Biology, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationotherHoward Hughes Medical Institute, Department of Anatomy, University of California, San Francisco, San Francisco, California 94143en_US
dc.contributor.affiliationotherHoward Hughes Medical Institute, Department of Anatomy, University of California, San Francisco, San Francisco, California 94143en_US
dc.contributor.affiliationotherHarvard University, Department of Cellular and Developmental Biology, Biological Laboratories, Cambridge, Massachusetts 02138en_US
dc.contributor.affiliationotherHarvard University, Department of Cellular and Developmental Biology, Biological Laboratories, Cambridge, Massachusetts 02138en_US
dc.identifier.pmid8906497en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50070/1/7_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/(SICI)1096-9861(19961014)374:2<246::AID-CNE7>3.0.CO;2-2en_US
dc.identifier.sourceThe Journal of Comparative Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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