Moving the research forward : the best of British biology using the tractable model system Dictyostelium discoideum

The social amoeba Dictyostelium discoideum provides an excellent model for research across a broad range of disciplines within biology. The organism diverged from the plant, yeast, fungi and animal kingdoms around 1 billion years ago but retains common aspects found in these kingdoms. Dictyostelium has a low level of genetic complexity and provides a range of molecular, cellular, biochemical and developmental biology experimental techniques, enabling multidisciplinary studies to be carried out in a wide range of areas, leading to research breakthroughs. Numerous laboratories within the United Kingdom employ Dictyostelium as their core research model. This review introduces Dictyostelium and then highlights research from several leading British research laboratories, covering their distinct areas of research, the benefits of using the model, and the breakthroughs that have arisen due to the use of Dictyostelium as a tractable model system

Cysteine proteinase 2 : structure and expression of a developmentally regulated gene of Dictyostelium discoideum

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Protein Kinase Cε Actin-binding Site Is Important for Neurite Outgrowth during Neuronal Differentiation

We have previously shown that protein kinase Cε (PKCε) induces neurite outgrowth via its regulatory domain and independently of its kinase activity. This study aimed at identifying mechanisms regulating PKCε-mediated neurite induction. We show an increased association of PKCε to the cytoskeleton during neuronal differentiation. Furthermore, neurite induction by overexpression of full-length PKCε is suppressed if serum is removed from the cultures or if an actin-binding site is deleted from the protein. A peptide corresponding to the PKCε actin-binding site suppresses neurite outgrowth during neuronal differentiation and outgrowth elicited by PKCε overexpression. Neither serum removal, deletion of the actin-binding site, nor introduction of the peptide affects neurite induction by the isolated regulatory domain. Membrane targeting by myristoylation renders full-length PKCε independent of both serum and the actin-binding site, and PKCε colocalized with F-actin at the cortical cytoskeleton during neurite outgrowth. These results demonstrate that the actin-binding site is of importance for signals acting on PKCε in a pathway leading to neurite outgrowth. Localization of PKCε to the plasma membrane and/or the cortical cytoskeleton is conceivably important for its effect on neurite outgrowth