Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-10-30
pubmed:abstractText
G protein Galpha subunits contribute to the specificity of different signal transduction pathways in Dictyostelium discoideum but Galpha subunit-effector interactions have not been previously identified. The requirement of the Dictyostelium Galpha4 subunit for MAP kinase (MAPK) activation and the identification of a putative MAPK docking site (D-motif) in this subunit suggested a possible interaction between the Galpha4 subunit and MAPKs. In vivo association of the Galpha4 subunit and ERK2 was demonstrated by pull-down and co-immunoprecipitation assays. Alteration of the D-motif reduced Galpha4 subunit-ERK2 interactions but only slightly altered MAPK activation in response to folate. Expression of the Galpha4 subunit with the altered D-motif in galpha4(-)cells allowed for slug formation but not the morphogenesis associated with culmination. Expression of this mutant Galpha4 subunit was sufficient to rescue chemotactic movement to folate. Alteration of the D-motif also reduced the aggregation defect associated with constitutively active Galpha4 subunits. These results suggest Galpha4 subunit-MAPK interactions are necessary for developmental morphogenesis but not for chemotaxis to folate.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1095-564X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
335
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
385-95
pubmed:dateRevised
2010-12-3
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
The Galpha4 G protein subunit interacts with the MAP kinase ERK2 using a D-motif that regulates developmental morphogenesis in Dictyostelium.
pubmed:affiliation
Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater, 74078-3020, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural