Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2003-8-5
pubmed:abstractText
During development of the Drosophila nervous system, kette is required for axonal growth and pathfinding. It encodes a highly conserved homolog of the Nck-associated protein 1 (NAP1) that genetically interacts with the Drosophila homolog of Nck, dock. We show that in vivo as well as in tissue culture models most of the Kette protein is found in the cytoplasm where it colocalizes with F-actin to which it can bind via its N-terminal domain. Some Kette protein is localized at the membrane and accumulates at focal contact sites. Loss of Kette protein results in the accumulation of cytosolic F-actin. The kette mutant phenotype can be suppressed by reducing the wave gene dose, demonstrating that kette antagonizes wave function. Overexpression of the wild-type Kette protein does not interfere with normal development, whereas expression of an activated, membrane-tethered Kette protein induces the formation of large F-actin bundles in both, tissue culture cells and in vivo. This gain-of-function phenotype is independent of wave but can be suppressed by reducing the wasp gene dose, indicating that Kette is able to regulate Wasp, to which it is linked via the Abelson interactor (Abi). Our data suggest a model where Kette fulfils a novel role in regulating F-actin organization by antagonizing Wave and activating Wasp-dependent actin polymerization.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
130
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4427-37
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Kette regulates actin dynamics and genetically interacts with Wave and Wasp.
pubmed:affiliation
Institut für Neurobiologie, Universität Münster, D-48149 Münster, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't