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dictyNews Volume 28 Number 11
dictyNews
Electronic Edition
Volume 28, number 11
May 4, 2007
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.
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Abstracts
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Stochastic signal processing and transduction in chemotactic response of
eukaryotic cells
Masahiro Ueda and Tatsuo Shibata
Laboratories for Nanobiology, Graduate School of Frontier Biosciences,
Osaka University, Suita, Osaka 565-0871, Japan
Department of Mathematical and Life Sciences, University of Hiroshima,
Higashi-Hiroshima, Hiroshima 739-8526, Japan
Biophysical Journal, in press
Single molecule imaging analysis of chemotactic response in eukaryotic cells
has revealed a stochastic nature in the input signals and the signal
transduction processes. This leads to a fundamental question on the signaling
processes: how does the signaling system operate under stochastic fluctuations
or noise? Here we report a stochastic model of chemotactic signaling in which
noise and signal propagation along transmembrane signaling by chemoattractant
receptors can be analyzed quantitatively. The results obtained from this
analysis reveal that the second messenger production reactions by the
receptors generate noisy signals, which contain intrinsic noise inherently
generated at this reaction and extrinsic noise propagated from the
ligand-receptor-binding. Such intrinsic and extrinsic noises limit directional
sensing ability of chemotactic cells, which can explain the dependence of
chemotactic accuracy on chemical gradients that have been observed
experimentally. Our analysis also reveals regulatory mechanisms for signal
improvements in the stochastically-operating signaling system by analyzing
how signal-to-noise ratio (SNR) of chemotactic signals can be improved or
deteriorated by the stochastic properties of receptors and second messenger
molecules. Theoretical consideration of noisy signal transduction by
chemotactic signaling systems can further be applied to other signaling
systems in general.
Submitted by: Masahiro Ueda [ueda@phys1.med.osaka-u.ac.jp]
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Input-output relationship in galvanotactic response
of Dictyostelium cells
Masayuki J. Sato, Michihito Ueda, Hiroaki Takagi, Tomonobu M. Watanabe,
Toshio Yanagida, and Masahiro Ueda
Laboratories for Nanobiology, Graduate School of Frontier Biosciences,
Osaka University, 1-3 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Advanced Technology Research Laboratories, Matsushita Electric Industrial Co.,
Ltd., 3-4 Hikaridai, Seika-cho, Soraku-gun, Kyoto 619-0237, Japan.
Biosystems 88, 261-272.
Under a direct current electric field, Dictyostelium cells exhibit migration
towards the cathode direction. To determine the input-output relationship of
the cellÕs galvanotactic response, we developed an experimental instrument in
which electric signals applied to the cells are highly reproducible and the
motile response are analyzed quantitatively. With no electric field, the cells
moved randomly in all directions. Upon applying an electric field, cell
migration speeds became about 1.3 times faster than those in the absence of an
electric field. Such kinetic effects of electric fields on the migration were
observed for cells stimulated between 0.25 to 10 V/cm of the field strength.
The directions of cell migrations were biased toward the cathode in a positive
manner with field strength, showing galvanotactic response in a dose-dependent
manner. Quantitative analysis of the relationship between field strengths and
directional movements revealed that the biased movements of the cells depend on
the square of electric field strength, which can be described by one simple
phenomenological equation. The threshold strength for the galvanotaxis was
between 0.25 and 1 V/cm. Galvanotactic efficiency reached to half-maximum at
2.6 V/cm, which corresponds to an approximately 8 mV voltage difference between
the cathode and anode direction of 10 microm wide, round cells. Based on these
results, possible mechanisms of galvanotaxis in Dictyostelium cells were
discussed. This development of experimental system, together with its good
microscopic accessibility for intracellular signaling molecules, makes
Dictyostelium cells attractive as a model organism for elucidating stochastic
processes in the signaling systems responsible for cell motility and its
regulations.
Submitted by: Masahiro Ueda [ueda@phys1.med.osaka-u.ac.jp]
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Dictyostelium differentiation-inducing factor-1 (DIF-1) induces GLUT1
translocation and promotes glucose uptake in mammalian cells
Waka Omata, Hiroshi Shibata, Msahiro Nagasawa, Itaru Kojima, Haruhisa Kikuchi,
Yoshiteru Oshima, Kohei Hosaka and Yuzuru Kubohara
Institute for Molecular and Cellular Regulation, Gunma University, Janan.
FEBS Journal, In press
The differentiation-inducing factor-1 (DIF-1) is a signal molecule that induces
stalk cell formation in the cellular slime mold Dictyostelium discoideum, while
DIF-1 and its analogs have been shown to possess anti-proliferative activity
in vitro in mammalian tumor cells. In the present study, we have investigated
the effects of DIF-1 and its analogs on normal (non-transformed) mammalian cells.
Without affecting the cell morphology and cell number, DIF-1 at micromolar levels
dose-dependently promoted the glucose uptake in confluent 3T3-L1 fibroblasts,
which was not inhibited with wortmannin or LY293002 [inhibitors for
phosphatidylinositol 3-kinase (PI3K)]. DIF-1 affected neither the expression
level of GLUT1 (glucose transporter 1) nor the activities of four key enzymes
involved in glucose metabolism, such as hexokinase, fluctose-6-phosphate kinase,
pyruvate kinase, and glucose-6-phosphate dehydrogenase. Most importantly,
stimulation with DIF-1 was found to induce the translocation of GLUT1 from
intracellular vesicles to the plasma membranes in the cells. In differentiated
3T3-L1 adipocytes, DIF-1 induced the translocation of GLUT1 (but not of GLUT4)
and promoted glucose uptake, which was not inhibited with wortmannin. These
results indicate that DIF-1 induces GLUT1 translocation and thereby promotes
glucose uptake, at least in part, via a PI3K/Akt-independent pathway in mammalian
cells. Furthermore, analogs of DIF-1 that possess stronger anti-tumor activity
than DIF-1 were less effective in promoting glucose consumption, suggesting that
the mechanism of the action of DIF-1 for stimulating glucose uptake should be
different from that for suppressing tumor cell growth.
Submitted by: Yuzuru Kubohara [kubohara@showa.gunma-u.ac.jp]
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[End dictyNews, volume 28, number 11]
