Show simple item record

dc.contributor.authorSchwarting, Gerald A.
dc.contributor.authorHenion, Timothy R.
dc.date2022-08-11T08:10:52.000
dc.date.accessioned2022-08-23T17:23:17Z
dc.date.available2022-08-23T17:23:17Z
dc.date.issued2007-10-15
dc.date.submitted2011-03-22
dc.identifier.citationDev Neurobiol. 2007 Oct;67(12):1627-40. <a href="http://dx.doi.org/10.1002/dneu.20536">Link to article on publisher's site</a>
dc.identifier.issn1932-8451 (Linking)
dc.identifier.doi10.1002/dneu.20536
dc.identifier.pmid17567839
dc.identifier.urihttp://hdl.handle.net/20.500.14038/48923
dc.description.abstractDuring embryonic development, olfactory sensory neurons extend axons that form synapses with the dendrites of projection neurons in glomeruli of the olfactory bulb (OB). The glycosyltransferase beta3GnT1 regulates the expression of 1B2-reactive lactosamine glycans that are mosaically distributed among glomeruli. In newborn beta3GnT1-/- mice, lactosamine expression is lost, and many glomeruli fail to form. To determine the role of lactosamine in OB targeting, we analyzed the trajectories of specific OR axon populations and their reactivity with 1B2 in beta3GnT1-/- mice. mI7 axons and P2 axons, both of which are weakly 1B2+ in wild-type mice, fail to grow to their normal positions in the glomerular layer during early postnatal development and never recover in adult mutant mice. In contrast, many M72 axons, which are always lactosamine negative in wild-type mice, survive but are misguided to the extreme anterior OB in neonatal mutant mice and persist as heterotypic glomeruli, even in adult null mice. These results show that the loss of lactosamine differentially affects each OR population. Those that lose their normal expression of lactosamine fail to form stable connections with mitral and tufted cells in the OB, disappear during early postnatal development, and do not recover in adults. Neurons that are normally lactosamine negative, survive early postnatal degeneration in beta3GnT1-/- mice but extend axons that converge on inappropriate targets in the mutant OB.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17567839&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/dneu.20536
dc.subjectAmino Sugars
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectAxons
dc.subjectGlycosyltransferases
dc.subjectImmunohistochemistry
dc.subjectMice
dc.subjectMice, Mutant Strains
dc.subjectNeurons, Afferent
dc.subjectOlfactory Bulb
dc.subjectOlfactory Pathways
dc.subjectCell Biology
dc.titleLactosamine differentially affects olfactory sensory neuron projections to the olfactory bulb
dc.typeJournal Article
dc.source.journaltitleDevelopmental neurobiology
dc.source.volume67
dc.source.issue12
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/schwarting/4
dc.identifier.contextkey1892447
html.description.abstract<p>During embryonic development, olfactory sensory neurons extend axons that form synapses with the dendrites of projection neurons in glomeruli of the olfactory bulb (OB). The glycosyltransferase beta3GnT1 regulates the expression of 1B2-reactive lactosamine glycans that are mosaically distributed among glomeruli. In newborn beta3GnT1-/- mice, lactosamine expression is lost, and many glomeruli fail to form. To determine the role of lactosamine in OB targeting, we analyzed the trajectories of specific OR axon populations and their reactivity with 1B2 in beta3GnT1-/- mice. mI7 axons and P2 axons, both of which are weakly 1B2+ in wild-type mice, fail to grow to their normal positions in the glomerular layer during early postnatal development and never recover in adult mutant mice. In contrast, many M72 axons, which are always lactosamine negative in wild-type mice, survive but are misguided to the extreme anterior OB in neonatal mutant mice and persist as heterotypic glomeruli, even in adult null mice. These results show that the loss of lactosamine differentially affects each OR population. Those that lose their normal expression of lactosamine fail to form stable connections with mitral and tufted cells in the OB, disappear during early postnatal development, and do not recover in adults. Neurons that are normally lactosamine negative, survive early postnatal degeneration in beta3GnT1-/- mice but extend axons that converge on inappropriate targets in the mutant OB.</p>
dc.identifier.submissionpathschwarting/4
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentEunice Kennedy Shriver Center
dc.source.pages1627-40


This item appears in the following Collection(s)

Show simple item record