Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23
pubmed:dateCreated
1997-12-15
pubmed:abstractText
The reeler mutation in mice produces an especially well characterized disorder, with systematically abnormal migration of cerebral cortical neurons. The reeler gene encodes a large protein, termed Reelin, that in the cortex is synthesized and secreted exclusively in the Cajal-Retzius neurons of the cortical marginal zone (D'Arcangelo et al., 1995). In reeler mutant mice, loss of Reelin protein is associated with a systematic loss of the normal, "inside-out" sequence of neurogenesis in the cortex: neurons are formed in the normal sequence but become localized in the cortex in a somewhat inverted, although relatively disorganized "outside-in" pattern. Here we show that the scrambler mutant mouse exhibits a loss of lamination in the cortex and hippocampus that is indistinguishable from that seen in the reeler mouse. We use BrdU birthdating studies to show that scrambler cortex shows a somewhat inverted "outside-in" sequence of birthdates for cortical neurons that is similar to that previously described in reeler cortex. Finally, we perform staining with the CR-50 monoclonal antibody (Ogawa et al., 1995), which recognizes the Reelin protein (D'Arcangelo et al., 1997). We show that Reelin immunoreactivity is present in the scrambler cortex in a normal pattern, suggesting that Reelin is synthesized and released normally. Our data suggest that scrambler is a mutation in the same gene pathway as the reeler gene (Relnrl) and is most likely downstream of Relnrl.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0270-6474
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9204-11
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9364067-Animals, pubmed-meshheading:9364067-Biological Markers, pubmed-meshheading:9364067-Cell Adhesion Molecules, Neuronal, pubmed-meshheading:9364067-Cell Lineage, pubmed-meshheading:9364067-Cell Movement, pubmed-meshheading:9364067-Cerebellar Cortex, pubmed-meshheading:9364067-Cerebral Cortex, pubmed-meshheading:9364067-Extracellular Matrix Proteins, pubmed-meshheading:9364067-Gene Expression Regulation, Developmental, pubmed-meshheading:9364067-Genetic Heterogeneity, pubmed-meshheading:9364067-Gestational Age, pubmed-meshheading:9364067-Hippocampus, pubmed-meshheading:9364067-Mice, pubmed-meshheading:9364067-Mice, Neurologic Mutants, pubmed-meshheading:9364067-Morphogenesis, pubmed-meshheading:9364067-Nerve Tissue Proteins, pubmed-meshheading:9364067-Neurons, pubmed-meshheading:9364067-Phenotype, pubmed-meshheading:9364067-Serine Endopeptidases
pubmed:year
1997
pubmed:articleTitle
Birthdate and cell marker analysis of scrambler: a novel mutation affecting cortical development with a reeler-like phenotype.
pubmed:affiliation
Division of Neurogenetics, Department of Neurology, Beth Israel Deaconess Medical Center, and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't