ArticleMicrobiology (Reading, England)2010
G{alpha}5 subunit-mediated signalling requires a D-motif and the MAPK ERK1 in Dictyostelium.
Article in Microbiology (Reading, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- MAPK docking motif in the Dictyostelium Gα2 subunit is required for aggregation and transcription factor translocation.Cellular signalling · 2021Article
- Article
- Pheromone-induced morphogenesis and gradient tracking are dependent on the MAPK Fus3 binding to Gα.Molecular biology of the cell · 2015Article
- The Dictyostelium MAPK ERK1 is phosphorylated in a secondary response to early developmental signaling.Cellular signalling · 2015Article
- MAPKs in development: insights from Dictyostelium signaling pathways.Biomolecular concepts · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Dictyostelium Galpha5 subunit has been shown to reduce cell viability, inhibit folate chemotaxis and accelerate tip morphogenesis and gene expression during multicellular development. Alteration of the D-motif (mitogen-activated protein kinase docking site) at the amino terminus of the Galpha 5 subunit or the loss of extracellular signal-regulated kinase (ERK)1 diminished the lethality associated with the overexpression or constitutive activation of the Galpha5 subunit. The amino-terminal D-motif of the Galpha5 subunit was also found to be necessary for the reduced cell size, small aggregate formation and precocious developmental gene expression associated with Galpha5 subunit overexpression. This D-motif also contributed to the aggregation delay in cells expressing a constitutively active Galpha5 subunit, but the D-motif was not necessary for the inhibition of folate chemotaxis. These results suggest that the amino-terminal D-motif is required for some but not all phenotypes associated with elevated Galpha5 subunit functions during growth and development and that ERK1 can function in Galpha5 subunit-mediated signal transduction.
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Registered trials
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