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dc.contributor.authorSchwarting, Gerald A.
dc.contributor.authorGridley, Thomas
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.issued2007-12-03
dc.date.submitted2011-03-22
dc.identifier.citationJ Mol Histol. 2007 Dec;38(6):543-53. Epub 2007 Jun 29. <a href="http://dx.doi.org/10.1007/s10735-007-9110-9">Link to article on publisher's site</a>
dc.identifier.issn1567-2379 (Linking)
dc.identifier.doi10.1007/s10735-007-9110-9
dc.identifier.pmid17605079
dc.identifier.urihttp://hdl.handle.net/20.500.14038/48922
dc.description.abstractDespite the relatively simplified organization of the olfactory epithelium (OE), our understanding of the factors that regulate its cellular diversity is limited. Genetic and localization studies suggest that Notch signaling may be important in this process. We characterize here a population of Notch1 (+) olfactory basal cells in embryonic mice that coordinately express both the Notch effector Hes5 and the glycosyltransferase Lfng. These cells are distinct from Mash1(+) neuronal precursors, but give rise to sensory neurons, suggesting that Notch1 signals may in part function to maintain a neurogenic progenitor pool. Furthermore, Lfng(+) cells also generate a population of cells in the migratory mass that appear to be ensheathing glial precursors, indicating potential multipotency in these progenitors. The Notch ligand Dll4 is expressed by basal OE cells that are interspersed with Notch1(+) progenitors during later OE neurogenesis. In contrast, mice deficient in Dll1 exhibit a smaller OE and a loss of Hes5 expression, indicating an earlier function in olfactory progenitor cell development. Taken together, these results further support a role for Notch signaling in the regulation of olfactory neurogenesis and cell diversity.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17605079&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1007/s10735-007-9110-9
dc.subjectAnimals
dc.subjectBasic Helix-Loop-Helix Transcription Factors
dc.subjectGene Expression
dc.subjectGlycosyltransferases
dc.subjectIntercellular Signaling Peptides and Proteins
dc.subjectIntracellular Signaling Peptides and Proteins
dc.subjectLigands
dc.subjectMembrane Proteins
dc.subjectMice
dc.subjectOlfactory Mucosa
dc.subjectReceptor, Notch1
dc.subjectRepressor Proteins
dc.subjectStem Cells
dc.subjectCell Biology
dc.titleNotch1 expression and ligand interactions in progenitor cells of the mouse olfactory epithelium
dc.typeJournal Article
dc.source.journaltitleJournal of molecular histology
dc.source.volume38
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/schwarting/3
dc.identifier.contextkey1892446
html.description.abstract<p>Despite the relatively simplified organization of the olfactory epithelium (OE), our understanding of the factors that regulate its cellular diversity is limited. Genetic and localization studies suggest that Notch signaling may be important in this process. We characterize here a population of Notch1 (+) olfactory basal cells in embryonic mice that coordinately express both the Notch effector Hes5 and the glycosyltransferase Lfng. These cells are distinct from Mash1(+) neuronal precursors, but give rise to sensory neurons, suggesting that Notch1 signals may in part function to maintain a neurogenic progenitor pool. Furthermore, Lfng(+) cells also generate a population of cells in the migratory mass that appear to be ensheathing glial precursors, indicating potential multipotency in these progenitors. The Notch ligand Dll4 is expressed by basal OE cells that are interspersed with Notch1(+) progenitors during later OE neurogenesis. In contrast, mice deficient in Dll1 exhibit a smaller OE and a loss of Hes5 expression, indicating an earlier function in olfactory progenitor cell development. Taken together, these results further support a role for Notch signaling in the regulation of olfactory neurogenesis and cell diversity.</p>
dc.identifier.submissionpathschwarting/3
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentEunice Kennedy Shriver Center
dc.source.pages543-53


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