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dictyNews Volume 39 Number 23
dictyNews
Electronic Edition
Volume 39, number 23
August 16, 2013
Please submit abstracts of your papers as soon as they have been
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or by using the form at
http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit.
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Abstracts
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The cyclin-dependent kinase family in the social amoebozoan
Dictyostelium discoideum
Robert J. Huber
Center for Human Genetic Research, Massachusetts General
Hospital, Harvard Medical School, Richard B. Simches Research
Center, 185 Cambridge Street, Boston, Massachusetts, USA 02114
Cellular and Molecular Life Sciences, in press
Cyclin-dependent kinases (Cdk) are a family of serine/threonine
protein kinases that regulate eukaryotic cell cycle progression.
Their ability to modulate the cell cycle has made them an attractive
target for anti-cancer therapies. Cdk protein function has been
studied in a variety of eukaryotes ranging from yeast to humans.
In the social amoebozoan Dictyostelium discoideum several
homologues of mammalian Cdks have been identified and
characterized. The life cycle of this model organism is comprised
of a feeding stage where single cells grow and divide mitotically as
they feed on their bacterial food source and a multicellular
developmental stage that is induced by starvation. Thus it is a
valuable system for studying a variety of cellular and developmental
processes. In this review I summarize the current knowledge of the
Cdk protein family in Dictyostelium by highlighting the research
efforts focused on the characterization of Cdk1, Cdk5, and Cdk8 in
this model eukaryote. Accumulated evidence indicates that each
protein performs distinct functions during the Dictyostelium life cycle
with Cdk1 being required for growth and Cdk5 and Cdk8 being
required for processes that occur during development. Recent
studies have shown that Dictyostelium Cdk5 shares attributes with
mammalian Cdk5 and that the mammalian Cdk inhibitor roscovitine
can be used to inhibit Cdk5 activity in Dictyostelium. Together, these
results show that Dictyostelium can be used as a model system for
studying Cdk protein function.
Submitted by "Robert J.Huber" [rhuber@chgr.mgh.harvard.edu]
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Loss of the Histidine Kinase DhkD Results in Mobile Mounds During
Development of Dictyostelium discoideum.
Charles K. Singleton and Yanhua Xiong
Department of Biological Sciences, Vanderbilt University
VU Station B 351634, Nashville, TN 37235-1634
PLOS ONE, in press
Background. Histidine kinases are receptors for sensing cellular and
environmental signals, and in response to the appropriate cue they
initiate phosphorelays that regulate the activity of response regulators.
The Dictyostelium discoideum genome encodes 15 histidine kinases
that function to regulate several processes during the multicellular
developmental program, including the slug to culmination transition,
osmoregulation, and spore differentiation. While there are many
histidine kinases, there is only a single response regulator, RegA.
Not surprisingly given the ubiquitous involvement of cAMP in
numerous processes of development in Dictyostelium, RegA is a
cAMP phosphodiesterase that is activated upon receiving phosphates
through a phosphorelay. Hence, all of the histidine kinases
characterized to date regulate developmental processes through
modulating cAMP production. Here we investigate the function of
the histidine kinase DhkD.
Principal Findings. The dhkD gene was disrupted, and the resulting
cells when developed gave a novel phenotype. Upon aggregation,
which occurred without streaming, the mounds were motile, a
phenotype termed the pollywog stage. The pollywog phenotype was
dependent on a functional RegA. After a period of random migration,
the pollywogs attempted to form fingers but mostly generated aberrant
structures with no tips. While prestalk and prespore cell differentiation
occurred with normal timing, proper patterning did not occur. In contrast,
wild type mounds are not motile, and the cAMP chemotactic movement
of cells within the mound facilitates proper prestalk and prespore
patterning, tip formation, and the vertical elongation of the mound
into a finger.
Conclusions. We postulate that DhkD functions to ensure the proper
cAMP distribution within mounds that in turn results in patterning, tip
formation and the transition of mounds to fingers. In the absence of
DhkD, aberrant cell movements in response to an altered cAMP
distribution result in mound migration, a lack of proper patterning, and
an inability to generate normal finger morphology.
Submitted by Charles Singleton [charles.k.singleton@vanderbilt.edu]
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[End dictyNews, volume 39, number 23]
