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dictyNews Volume 42 Number 19
dictyNews
Electronic Edition
Volume 42, number 19
August 12, 2016
Please submit abstracts of your papers as soon as they have been
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or by using the form at
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Abstracts
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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]
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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]
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[End dictyNews, volume 42, number 19]
