Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1997-1-30
pubmed:abstractText
A novel spontaneous neurological mutation, scrambler (scm), appeared in the inbred mouse strain DC/Le (dancer) in 1991. Mice homozygous for this recessive mutation are recognized by an unstable gait and whole-body tremor. The cerebella of 30-day-old scrambler homozygotes are hypoplastic and devoid of folia; however, neither seizures nor abnormal brain wave patterns have been observed. Homozygous scrambler mutants have an ataxic gait which in the male may be a contributory factor in the failure to mate. Female homozygotes mate and breed. Life span is not reduced in either sex. Scrambler is similar to the reeler mutation in phenotype and pathology and, like reeler, probably results from defective neuronal migration. We mapped the scrambler mutation to Chromosome (Chr) 4, proving that it is distinct from the recently cloned reeler gene on Chr 5. We also determined the map position of the agrin gene, Agrn, on Chr 4, and on this basis eliminated it as a candidate for scm. Currently there is no known homology of scrambler with human lissencephalies or other human disorders caused by abnormal neuronal migration.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0938-8990
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
798-802
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Scrambler, a new neurological mutation of the mouse with abnormalities of neuronal migration.
pubmed:affiliation
The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.