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rdf:type |
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lifeskim:mentions |
umls-concept:C0006772,
umls-concept:C0013138,
umls-concept:C0037083,
umls-concept:C0181586,
umls-concept:C0332453,
umls-concept:C0596632,
umls-concept:C0599894,
umls-concept:C0743559,
umls-concept:C1154402,
umls-concept:C1521840,
umls-concept:C1656935,
umls-concept:C1710082
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pubmed:issue |
1
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pubmed:dateCreated |
1995-2-22
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pubmed:abstractText |
Ca(2+)-calmodulin (CaM) function was selectively disrupted in a specific subset of growth cones in transgenic Drosophila embryos in which a specific enhancer element drives the expression of the kinesin motor domain fused to a CaM antagonist peptide (kinesin-antagonist or KA, which blocks CaM binding to target proteins) or CaM itself (kinesin-CaM or KC, which acts as a Ca(2+)-binding protein). In both KA and KC mutant embryos, specific growth cones exhibit dosage-dependent stalls in axon extension and errors in axon guidance, including both defects in fasciculation and abnormal crossings of the midline. These results demonstrate an in vivo function for Ca(2+)-CaM signaling in growth cone extension and guidance and suggest that Ca(2+)-CaM may in part regulate specific growth cone decisions, including when to defasciculate and whether or not to cross the midline.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0896-6273
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
43-56
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7826640-Amino Acid Sequence,
pubmed-meshheading:7826640-Animals,
pubmed-meshheading:7826640-Axons,
pubmed-meshheading:7826640-Base Sequence,
pubmed-meshheading:7826640-Blotting, Western,
pubmed-meshheading:7826640-Calcium,
pubmed-meshheading:7826640-Calmodulin,
pubmed-meshheading:7826640-Drosophila,
pubmed-meshheading:7826640-Gene Expression,
pubmed-meshheading:7826640-Genetic Engineering,
pubmed-meshheading:7826640-Kinesin,
pubmed-meshheading:7826640-Microtubules,
pubmed-meshheading:7826640-Molecular Sequence Data,
pubmed-meshheading:7826640-Neural Pathways,
pubmed-meshheading:7826640-Neurons,
pubmed-meshheading:7826640-Recombinant Fusion Proteins,
pubmed-meshheading:7826640-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:7826640-Signal Transduction,
pubmed-meshheading:7826640-beta-Galactosidase
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pubmed:year |
1995
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pubmed:articleTitle |
Targeted disruption of Ca(2+)-calmodulin signaling in Drosophila growth cones leads to stalls in axon extension and errors in axon guidance.
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pubmed:affiliation |
Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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