Linked Life Data

9675049

Source:http://linkedlifedata.com/resource/pubmed/id/9675049

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-9-25
pubmed:abstractText
The semaphorins constitute a large gene family of transmembrane and secreted molecules, many of which are expressed in the nervous system. Genetic studies in Drosophila have revealed a role for semaphorins in axon guidance and synapse formation, and several in vitro studies in mice have demonstrated a dramatic chemorepellent effect of semaphorin III (Sema III) on the axons of several populations of neurons. To investigate the function of Sema III during in vivo axon guidance in the mammalian CNS, we studied the development of axonal projections in mutant mice lacking Sema III. Projections were studied for which either the in vitro evidence suggests a role for Sema III in axon guidance (e.g., cerebellar mossy fibers, thalamocortical axons, or cranial motor neurons) or the in vivo expression suggests a role for Sema III in axon guidance (e.g., cerebellar Purkinje cells, neocortex). We find that many major axonal projections, including climbing fiber, mossy fiber, thalamocortical, and basal forebrain projections and cranial nerves, develop normally in the absence of Sema III. Despite its in vitro function and in vivo expression, it appears as if Sema III is not absolutely required for the formation of many major CNS tracts. Such data are consistent with recent models suggesting that axon guidance is controlled by a balance of forces resulting from multiple guidance cues. Our data lead us to suggest that if Sema III functions in part to guide the formation of major axonal projections, then it does so in combination with both other semaphorins and other families of guidance molecules.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1044-7431
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Academic Press.
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
173-82
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9675049-Animals, pubmed-meshheading:9675049-Axons, pubmed-meshheading:9675049-Biological Markers, pubmed-meshheading:9675049-Brain, pubmed-meshheading:9675049-Calcitonin Gene-Related Peptide, pubmed-meshheading:9675049-Calcium-Binding Protein, Vitamin D-Dependent, pubmed-meshheading:9675049-Cerebral Cortex, pubmed-meshheading:9675049-Glycoproteins, pubmed-meshheading:9675049-In Situ Hybridization, pubmed-meshheading:9675049-Mesencephalon, pubmed-meshheading:9675049-Mice, pubmed-meshheading:9675049-Mice, Knockout, pubmed-meshheading:9675049-Morphogenesis, pubmed-meshheading:9675049-Motor Neurons, pubmed-meshheading:9675049-Nerve Fibers, pubmed-meshheading:9675049-Nerve Growth Factors, pubmed-meshheading:9675049-Purkinje Cells, pubmed-meshheading:9675049-Pyramidal Cells, pubmed-meshheading:9675049-RNA, Messenger, pubmed-meshheading:9675049-Rhombencephalon, pubmed-meshheading:9675049-Semaphorin-3A, pubmed-meshheading:9675049-Thalamus
pubmed:year
1998
pubmed:articleTitle
Many major CNS axon projections develop normally in the absence of semaphorin III.
pubmed:affiliation
Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, 94720-3200, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't