dictyNews
Electronic Edition
Volume 42, number 19
August 12, 2016

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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 [[log in to unmask]]
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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 [[log in to unmask]]
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[End dictyNews, volume 42, number 19]