ArticleBMC developmental biology2004
A link of Ca2+ to cAMP oscillations in Dictyostelium: the calmodulin antagonist W-7 potentiates cAMP relay and transiently inhibits the acidic Ca2+-store.
Article in BMC developmental biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Establishing functional giant Dictyostelium cells reveals front-rear polarity in intracellular signaling.Communications biology · 2026Article
- Intracellular Calcium Responses to External Calcium Stimuli inJournal of microbiology and biotechnology · 2025Article
- Ion Signaling in Cell Motility and Development inBiomolecules · 2024Review
- Calmodulin-mediated events during the life cycle of the amoebozoan Dictyostelium discoideum.Biological reviews of the Cambridge Philosophical Society · 2020Review
- Calmodulin and Calmodulin Binding Proteins inInternational journal of molecular sciences · 2020Review
- Acidic Ca2+ stores, excitability, and cell patterning in Dictyostelium discoideum.Eukaryotic cell · 2009Review
- The contractile vacuole in Ca2+-regulation in Dictyostelium: its essential function for cAMP-induced Ca2+-influx.BMC developmental biology · 2006Article
- Release of Ca2+ from the endoplasmic reticulum contributes to Ca2+ signaling in Dictyostelium discoideum.Eukaryotic cell · 2005Article
- cAMP controls cytosolic Ca2+ levels in Dictyostelium discoideum.BMC cell biology · 2005Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDuring early differentiation of Dictyostelium the attractant cAMP is released periodically to induce aggregation of the cells. Here we pursue the question whether pulsatile cAMP signaling is coupled to a basic Ca2+-oscillation.
resultsWe found that the calmodulin antagonist W-7 transiently enhanced cAMP spikes. We show that W-7 acts on an acidic Ca2+-store: it abolished ATP-dependent vesicular acidification, inhibited V-type H+ATPase activity more potently than the weaker antagonist W-5 and caused vesicular Ca2+-leakage. Concanamycin A, an inhibitor of the V-type H+-pump, blocked the Ca2+-leakage elicited by W-7 as well as cAMP-oscillations in the presence of W-7. Concanamycin A caused an increase of the cytosolic Ca2+-concentration whereas W-7 did not. In case of the latter, Ca2+ was secreted by the cells. In accord with our hypothesis that the link from Ca2+ to cAMP synthesis is mediated by a Ca2+-dependent phospholipase C we found that W-7 was not active in the phospholipase C knockout mutant.
conclusionWe conclude that the potentiation of cAMP relay by W-7 is due to a transient inhibition of the acidic Ca2+-store. The inhibition of the proton pump by W-7 causes a leakage of Ca2+ that indirectly stimulates adenylyl cyclase activity via phospholipase C.
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