dictyNews
Electronic Edition
Volume 34, number 3
January 22, 2010
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Abstracts
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A coronin7 homolog with functions in actin-driven processes
Maria C. Shina, Can Ünal, Ludwig Eichinger, Annette Müller-Taubenberger,
Michael Schleicher, Michael Steinert, Angelika A. Noegel
J. Biol. Chem., in press
Dictyostelium discoideum Coronin7 (DdCRN7) together with human
Coronin7 (CRN7) and Pod-1 of Drosophila melanogaster and
Caenorhabditis elegans belong to the coronin family of WD repeat
domain containing proteins. Coronin7 proteins are characterized by two
WD repeat domains that presumably fold into two beta-propeller
structures.
DdCRN7 shares highest homology with human CRN7, a protein with roles
in membrane trafficking. DdCRN7 is present in the cytosol and
accumulates
in cell surface projections during movement and phago- and pinocytosis.
Cells lacking CRN7 have altered chemotaxis and phagocytosis.
Furthermore,
loss of CRN7 affects the infection process by the pathogen Legionella
pneumophila and allows a more efficient internalization of bacteria. To
provide a mechanism for CNR7 action we studied actin related aspects.
We could show that CRN7 binds directly to F-actin and protects actin
filaments from depolymerization. CRN7 also associated with F-actin in
vivo. It was present in the Triton X-100 insoluble cytoskeleton,
colocalized
with F-actin and its distribution was sensitive to drugs affecting the
actin
cytoskeleton. We propose that CRN7's role in chemotaxis and
phagocytosis is through its effect on the actin cytoskeleton.
Submitted by Angelika Noegel [[log in to unmask]]
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Cheating by Exploitation of Developmental Prestalk Patterning in
Dictyostelium discoideum
Anupama Khare and Gad Shaulsky; Department of Molecular and Human
Genetics, Baylor College of Medicine, Houston, Texas, USA
PLoS Genetics, in press
The cooperative developmental system of the social amoeba Dictyostelium
discoideum is susceptible to exploitation by cheaters – strains that
make
more than their fair share of spores in chimerae. Laboratory screens in
Dictyostelium have shown that the genetic potential for facultative
cheating
is high and field surveys have shown that cheaters are abundant in
nature,
but the cheating mechanisms are largely unknown. Here we describe
cheater C (chtC), a strong facultative cheater mutant that cheats by
affecting prestalk differentiation. The chtC gene is developmentally
regulated and its mRNA becomes stalk-enriched at the end of development.
chtC mutants are defective in maintaining the prestalk cell fate as
some of
their prestalk cells transdifferentiate into prespore cells, but that
defect
does not affect gross developmental morphology or sporulation
efficiency.
In chimerae between wild-type and chtC mutant cells, the wild-type cells
preferentially give rise to prestalk cells, and the chtC mutants
increase
their representation in the spore mass. Mixing chtC mutants with other
cell-type proportioning mutants revealed that the cheating is directly
related to the prestalk-differentiation propensity of the victim. These
findings illustrate that a cheater can victimize cooperative strains by
exploiting an established developmental pathway.
Submitted by Gad Shaulsky [[log in to unmask]]
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