ArticlePloS one2014
The hybrid type polyketide synthase SteelyA is required for cAMP signalling in early Dictyostelium development.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Global profiling of polyketide synthases in facultative multicellular eukaryotes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Yellow polyketide pigment suppresses premature hatching in social amoeba.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Evolution and Diversity of Assembly-Line Polyketide Synthases.Chemical reviews · 2019Review
- Proteomic and Transcriptomic Profiling Identifies Early Developmentally Regulated Proteins inCells · 2019Article
- 4-Methyl-5-Pentylbenzene-1,3-Diol Regulates Chemotactic Cell Aggregation and Spore Maturation Via Different Mechanisms in Dictyostelium discoideum.Current microbiology · 2019Article
- Evolution of multicellularity in Dictyostelia.The International journal of developmental biology · 2019Review
- D-Serine Metabolism and Its Importance in Development ofFrontiers in microbiology · 2018Article
- A polycystin-type transient receptor potential (Trp) channel that is activated by ATP.Biology open · 2017Article
- Evolution of developmental signalling in Dictyostelid social amoebas.Current opinion in genetics & development · 2016Review
- The Evolution of Aggregative Multicellularity and Cell-Cell Communication in the Dictyostelia.Journal of molecular biology · 2015Review
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Authors and funding
4 authors.
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Abstract
backgroundIn our previous study we found that the expression of stlA showed peaks both in the early and last stages of development and that a product of SteelyA, 4-methyl-5-pentylbenzene-1,3-diol (MPBD), controlled Dictyostelium spore maturation during the latter. In this study we focused on the role of SteelyA in early stage development. PRINCIPAL
findingsOur stlA null mutant showed aggregation delay and abnormally small aggregation territories. Chemotaxis analysis revealed defective cAMP chemotaxis in the stlA null mutant. cAMP chemotaxis was restored by MPBD addition during early stage development. Assay for cAMP relay response revealed that the stlA null mutant had lower cAMP accumulation during aggregation, suggesting lower ACA activity than the wild type strain. Exogenous cAMP pulses rescued the aggregation defect of the stlA null strain in the absence of MPBD. Expression analysis of cAMP signalling genes revealed lower expression levels in the stlA null mutant during aggregation.
conclusionOur data indicate a regulatory function by SteelyA on cAMP signalling during aggregation and show that SteelyA is indispensable for full activation of ACA.
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