Browse
Submit Data
Databases
API
Help

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chemoattractants induce tyrosine phosphorylation of ERK2 in Dictyostelium discoideum by diverse signalling pathways.

ABSTRACT: Two homologues of mitogen-activated protein kinases have been identified in Dictyostelium discoideum (ERK1 and EKR2). We here demonstrate transient tyrosine phosphorylation of ERK2 in response to the chemoattractants cAMP and folic acid that correlates with activity. To investigate the signalling pathways, we studied the response in strains with altered cAMP-dependent protein kinase (PKA) status. The degree of cAMP-induced ERK2 tyrosine phosphorylation was increased in cells overexpressing PKA activity but no such increase was observed in the response to folic acid. Our observations suggest that cAMP-induced ERK2 tyrosine phosphorylation is positively modulated by a PKA-regulated step which is not involved in the response to folic acid, suggesting the presence of diverse signalling pathways leading to ERK2 activation.

SUBMITTER: Kosaka C

PROVIDER: S-EPMC1218436 | biostudies-other | 1997 May

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Four key signaling pathways mediating chemotaxis in Dictyostelium discoideum.

Project description:Chemotaxis is the ability of cells to move in the direction of an external gradient of signaling molecules. Cells are guided by actin-filled protrusions in the front, whereas myosin filaments retract the rear of the cell. Previous work demonstrated that chemotaxis of unpolarized amoeboid Dictyostelium discoideum cells is mediated by two parallel pathways, phosphoinositide-3-kinase (PI3K) and phospholipase A2 (PLA2). Here, we show that polarized cells exhibit very good chemotaxis with inhibited PI3K and PLA2 activity. Using genetic screens, we demonstrate that this activity is mediated by a soluble guanylyl cyclase, providing two signals. The protein localizes to the leading edge where it interacts with actin filaments, whereas the cyclic guanosine monophosphate product induces myosin filaments in the rear of the cell. We conclude that chemotaxis is mediated by multiple signaling pathways regulating protrusions at the front and rear of the cell. Cells that express only rear activity are polarized but do not exhibit chemotaxis, whereas cells with only front signaling are unpolarized but undergo chemotaxis.

| S-EPMC2265585 | biostudies-literature

Salmonella infected Dictyostelium discoideum

Project description:This SuperSeries is composed of the SubSeries listed below.

2010-03-10 | GSE20688 | GEO

Developmental commitment in Dictyostelium discoideum.

Project description:Upon starvation, Dictyostelium discoideum cells halt cell proliferation, aggregate into multicellular organisms, form migrating slugs, and undergo morphogenesis into fruiting bodies while differentiating into dormant spores and dead stalk cells. At almost any developmental stage cells can be forced to dedifferentiate when they are dispersed and diluted into nutrient broth. However, migrating slugs can traverse lawns of bacteria for days without dedifferentiating, ignoring abundant nutrients and continuing development. We now show that developing Dictyostelium cells revert to the growth phase only when bacteria are supplied during the first 4 to 6 h of development but that after this time, cells continue to develop regardless of the presence of food. We postulate that the cells' inability to revert to the growth phase after 6 h represents a commitment to development. We show that the onset of commitment correlates with the cells' loss of phagocytic function. By examining mutant strains, we also show that commitment requires extracellular cyclic AMP (cAMP) signaling. Moreover, cAMP pulses are sufficient to induce both commitment and the loss of phagocytosis in starving cells, whereas starvation alone is insufficient. Finally, we show that the inhibition of development by food prior to commitment is independent of contact between the cells and the bacteria and that small soluble molecules, probably amino acids, inhibit development during the first few hours and subsequently the cells become unable to react to the molecules and commit to development. We propose that commitment serves as a checkpoint that ensures the completion of cooperative aggregation of developing Dictyostelium cells once it has begun, dampening the response to nutritional cues that might inappropriately block development.

| S-EPMC2168402 | biostudies-literature

Dictyostelium discoideum

Project description:Differential expression of Dictyostelium discoideum AX2 upon infection with wt L. pneumophila JR32 vs. L. hackeliae 24h p.i.

| PRJNA218463 | ENA

Dictyostelium discoideum

Project description:D. discoideum NC4 transcriptome data

| PRJNA80129 | ENA

Dictyostelium discoideum

Project description:Social amoeba that is a powerful model organism for studying cellular and developmental processes

| PRJNA9565 | ENA

Dictyostelium discoideum

Project description:Differential Expression upon infection with Salmonella typhimurium (t1)

| PRJNA129603 | ENA

Dictyostelium discoideum

Project description:Analysis of Biological Soliton

| PRJDB3922 | ENA

Dictyostelium discoideum

Project description:The retinoblastoma orthologue, rblA, is a major regulator of S-phase, mitotic, and developmental gene expression in Dictyostelium

| PRJNA143419 | ENA

Dictyostelium discoideum

Project description:Differential expression of Dictyostelium discoideum AX2 upon infection with wt L. pneumophila JR32 vs. uninfected 6h p.i. (timecourse experiment)

| PRJNA221555 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data