Linked Life Data

12629181

Source:http://linkedlifedata.com/resource/pubmed/id/12629181

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-3-11
pubmed:abstractText
MASH1, a basic helix-loop-helix transcription factor, is widely expressed by neuronal progenitors in the CNS and PNS, suggesting that it plays a role in the development of many neural regions. However, in mice lacking a functional Mash1 gene, major alterations have been reported in only a few neuronal populations; among these is a generalized loss of olfactory receptor neurons of the olfactory epithelium. Here, we use a transgenic reporter mouse line, in which the cell bodies and growing axons of subsets of central and peripheral neurons are marked by expression of a tau-lacZ reporter gene (the Tattler-4 allele), to look both more broadly and deeply at defects in the nervous system of Mash1-/- mice. In addition to the expected lack of olfactory receptor neurons in the main olfactory epithelium, developing Mash1-/-;Tattler-4+/- mice exhibited reductions in neuronal cell number in the vomeronasal organ and in the olfactory bulb; the morphology of the rostral migratory stream, which gives rise to olfactory bulb interneurons, was also abnormal. Further examination of cell proliferation, cell death, and cell type-specific markers in Mash1-/- animals uncovered parallels between the main olfactory epithelium and the vomeronasal organ in the regulation of sensory neuron development. Interestingly, this analysis also revealed that, in the olfactory epithelium of Mash1-/- animals, there is an overproduction of proliferating cells that co-express markers of both neuronal progenitors and supporting cells. This finding suggests that olfactory receptor neurons and olfactory epithelium supporting cells may share a common progenitor, and that expression of Mash1 may be an important factor in determining whether these progenitors ultimately generate neurons or glia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1769-80
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12629181-Animals, pubmed-meshheading:12629181-Antigens, Differentiation, pubmed-meshheading:12629181-Apoptosis, pubmed-meshheading:12629181-Axons, pubmed-meshheading:12629181-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:12629181-Bromodeoxyuridine, pubmed-meshheading:12629181-Cell Division, pubmed-meshheading:12629181-Cell Movement, pubmed-meshheading:12629181-DNA-Binding Proteins, pubmed-meshheading:12629181-Galactosidases, pubmed-meshheading:12629181-Genes, Reporter, pubmed-meshheading:12629181-Immunohistochemistry, pubmed-meshheading:12629181-In Situ Hybridization, pubmed-meshheading:12629181-Lateral Ventricles, pubmed-meshheading:12629181-Mice, pubmed-meshheading:12629181-Mice, Transgenic, pubmed-meshheading:12629181-Nervous System Malformations, pubmed-meshheading:12629181-Olfactory Bulb, pubmed-meshheading:12629181-Olfactory Mucosa, pubmed-meshheading:12629181-Olfactory Pathways, pubmed-meshheading:12629181-Olfactory Receptor Neurons, pubmed-meshheading:12629181-Stem Cells, pubmed-meshheading:12629181-Transcription Factors, pubmed-meshheading:12629181-Tubulin, pubmed-meshheading:12629181-Vomeronasal Organ
pubmed:year
2003
pubmed:articleTitle
Widespread defects in the primary olfactory pathway caused by loss of Mash1 function.
pubmed:affiliation
Department of Anatomy and Neurobiology, Developmental Biology Center, University of California, Irvine, Irvine, California 92697-2300, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't