dictyNews Electronic Edition Volume 42, number 19 August 12, 2016 Please submit abstracts of your papers as soon as they have been accepted for publication by sending them to dicty@northwestern.edu or by using the form at http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit. Back issues of dictyNews, the Dicty Reference database and other useful information is available at dictyBase - http://dictybase.org. Follow dictyBase on twitter: http://twitter.com/dictybase ========= Abstracts ========= YelA, a putative Dictyostelium translational regulator, acts as an antagonist of DIF-1 signaling to control cell-type proportioning Yoko Yamada, Chris Sugden and Jeffrey G. Williams Int J Dev Biol., in press DIF-1 is a polyketide, that is produced by Dictyostelium prespore cells and that induces initially uncommitted cells to differentiate as prestalk cells. Exposure of cells to DIF-1 causes transitory hypo-phosphorylation of seven serine residues in YelA; a protein with a region of strong homology to the MIF4G domain of eukaryotic initiation factor eIF4G. Based upon its domain architecture, which in one important aspect closely resembles that of Death-Associated Protein 5 (DAP5), we predict a role in stimulating internal ribosome entry driven mRNA translation. The two paradigmatic DIF-1 inducible genes are ecmA and ecmB. In support of a YelA function in DIF-1 signaling, a YelA null strain shows greatly increased expression of ecmA and ecmB in response to DIF-1. Also, during normal development in the null strain, the two genes are accelerated in their expression. This is particularly evident for ecmB, a marker of stalk tube and supporting structure differentiation. Mutants in DIF-1 bio- synthesis or signaling display a rudimentary or no basal disc and, conversely, YelA null mutants produce fruiting bodies with a highly enlarged basal disc that ectopically expresses a stalk tube-specific marker. Thus YelA acts as an antagonist of DIF-1 signaling, with a consequent effect on cell type proportioning and it is predicted to act as a translational regulator. submitted by: Yoko Yamada [y.yamada@dundee.ac.uk] ——————————————————————————————————————— Extracellular polyphosphate inhibits proliferation in an autocrine negative feedback loop in Dictyostelium discoideum Patrick M. Suess and Richard H. Gomer The Journal of Biological Chemistry, in press Polyphosphate is a polymer of phosphate residues linked by high-energy phosphoanhydride bonds. Despite being highly conserved throughout nature, its function is poorly understood. Here we show that Dictyostelium cells accumulate extracellular polyphosphate, and this acts to inhibit proliferation at high cell densities. In shaking culture, extracellular polyphosphate concentrations increase as cell density increases, and if the concentration of polyphosphate observed at stationary phase is added to cells at mid-log, proliferation is halted. Adding an exopolyphosphatase to cell cultures or stationary phase conditioned media decreases polyphosphate levels and abrogates the anti-proliferative effect. Cells show saturable binding of polyphosphate, suggesting the presence of a cell- surface polyphosphate receptor. Extracellular polyphosphate accumulation is potentiated by decreased nutrient levels, potentially as a means to anticipate starvation. Loss of the Dictyostelium polyphosphate kinase DdPpk1 causes intracellular polyphosphate levels to become undetectable, and negatively affects fitness, cytokinesis, and germination. However, cells lacking DdPpk1 accumulate ~50% normal levels of extracellular polyphosphate, suggesting an additional means of synthesis. We found that cells lacking inositol hexakisphosphate kinase, which is responsible for the synthesis of the inositol pyrophosphates IP7 and IP8, reach abnormally high cell densities and show decreased extracellular polyphosphate levels. Two different enzymes thus appear to mediate the synthesis of Dictyostelium extracellular polyphosphate, which is used as a signal in an autocrine negative feedback loop to regulate cell proliferation. submitted by: Patrick Suess [psuess@bio.tamu.edu] ============================================================== [End dictyNews, volume 42, number 19]