The protein kinase YakA regulates g-protein-linked signaling responses during growth and development of Dictyostelium.
A genetic screen for Dictyostelium mutants that phenotypically resemble cells lacking the G-protein beta-subunit yielded the protein kinase YakA. Like gbeta-null cells, yakA-null cells fail to enter development and display slow growth on bacterial lawns. We created a temperature-sensitive yakA mutant and showed that YakA activity is required not only at the onset but also during development. The yakA-null cells have strong defects in folic acid-induced responses, such as actin polymerization and cGMP accumulation, indicating that they play a role in G-protein-mediated signaling responses. We propose that YakA acts downstream of G-proteins, because cAMP receptors still couple to G-proteins in the yakA mutant. In addition, the previously observed growth arrest induced by overexpression of YakA also occurs in gbeta mutants. We localized YakA-GFP to the cytosol suggesting that YakA may be a functional homolog of its mammalian counterparts Dyrk2 and Dyrk3, a subclass of dual-specificity Yak-related kinases (Dyrk) with unknown function.
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Department of Cell Biology, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA.
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D000818:Animals; D017868:Cyclic AMP-Dependent Protein Kinases / Q000502:physiology; D003600:Cytosol / Q000737:chemistry; D004023:Dictyostelium / Q000254:growth & development*; D005492:Folic Acid / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000502:physiology*; D011494:Protein Kinases / Q000502:physiology*; D015398:Signal Transduction
D005492:Folic Acid; D011494:Protein Kinases; C113280:YakA protein, Dictyostelium discoideum; D017868:Cyclic AMP-Dependent Protein Kinases; D019204:GTP-Binding Proteins