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dictyNews Volume 40 Number 23

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Published in 
Dicty News
 · 11 months ago

dictyNews 
Electronic Edition
Volume 40, number 23
September 12, 2014

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.

Follow dictyBase on twitter:
http://twitter.com/dictybase


=========
Abstracts
=========


The hybrid type polyketide synthase SteelyA is required for cAMP
signalling in early Dictyostelium development

Takaaki B. Narita, Zhi-hui Chen, Pauline Schaap and Tamao Saito


PLoS One, in press

BACK GROUND: In our previous study we found that the expression
of stlA showed peaks both in the early and last stages of development
and that a product of SteelyA, 4-methyl-5-pentylbenzene-1,3-diol
(MPBD), controlled Dictyostelium spore maturation during the latter. In
this study we focused on the role of SteelyA in early stage development.

PRINCIPAL FINDINGS: Our stlA null mutant showed aggregation delay
and abnormally small aggregation territories. Chemotaxis analysis
revealed defective cAMP chemotaxis in stlA null mutant. cAMP
chemotaxis was restored by MPBD addition during early stage
development. Assay for cAMP relay response revealed that the stlA null
mutant had lower cAMP accumulation during aggregation, suggesting
lower ACA activity than the wild type strain. Exogenous cAMP pulses
rescued the aggregation defect of the stlA null strain in the absence of
MPBD. Expression analysis of cAMP signalling genes revealed lower
expression levels in stlA null mutant during aggregation.

CONCLUSION: Our data indicate a regulatory function by SteelyA on
cAMP signalling during aggregation and show that SteelyA is
indispensable for ACA full induction.


Submitted by Tamao Saito [tasaito@sophia.ac.jp]
---------------------------------------------------------------------------


Vmp1 regulates PtdIns3P signaling during autophagosome formation
in Dictyostelium discoideum

Javier Calvo-Garrido, Jason S. King, Sandra Mu–oz-Braceras and
Ricardo Escalante

Traffic, in press

Generation and turnover of PtdIns3P signaling is essential for
autophagosome formation and other membrane traffic processes.
In both Dictyostelium discoideum and mammalian cells,
autophagosomes are formed from specialized regions of the
endoplasmic reticulum (ER), called omegasomes, which are
enriched in the signaling lipid PtdIns3P. Vmp1 is a multi-spanning
membrane protein localized at the ER that is required for
autophagosome formation. There are conflicting reports in the
literature as to whether Vmp1 is strictly required or not for
autophagy-related PtdIns3P signaling and its hierarchical
relationship with Atg1 and PI3K. We have now addressed these
questions in the Dictyostelium model. We show that Dictyostelium
cells lacking Vmp1 have elevated and aberrant PtdIns3P signaling
on the ER, resulting in an increased and persistent recruitment of
Atg18 and other autophagic proteins. This indicates that Vmp1 is
not strictly essential for the generation of PtdIns3P signaling but
rather suggests a role in the correct turnover or modulation of this
signaling. Of interest, these PtdIns3P-enriched regions of the ER
surround ubiquitinated protein aggregates but are unable to form
functional autophagosomes. vmp1 null cells also have additional
defects in macropinocytosis and growth, that are not shared by
other autophagy mutants. Remarkably, we show that these defects
and also the aberrant PtdIns3P distribution are largely suppressed
by the concomitant loss of Atg1, indicating that aberrant autophagic
signaling on the ER inhibits macropinocytosis. These results
suggest that Atg1 functions upstream of Vmp1 in this signaling
pathway and demonstrates a previously unappreciated link
between abnormal autophagy signaling and macropinocytosis.


Submitted by Ricardo Escalante [rescalante@iib.uam.es]
---------------------------------------------------------------------------


Cellular memory in eukaryotic chemotaxis

Monica Skoge1,2 , Haicen Yue2 , Michael Erickstad2, Albert Bae1,2,
Herbert Levine3, Alex Groisman2, William F. Loomis1, and
Wouter-Jan Rappel2

1 Department of Biology, University of California San Diego,
La Jolla, CA 92093
2 Department of Physics, University of California San Diego,
La Jolla, CA 92093
3 Center for Theoretical Biological Physics and Department of
Bioengineering, Rice University, Houston, TX 77251


PNAS, in press

Natural chemical gradients to which cells respond chemotactically
are often dynamic, with both spatial and temporal components. A
primary example is the social amoeba Dictyostelium, which migrates
to the source of traveling waves of chemoattractant as part of a self-
organized aggregation process. Despite its physiological importance,
little is known about how cells migrate directionally in response to
traveling waves. The classic back-of-the-wave problem is how cells
chemotax towards the wave source, even though the spatial gradient
reverses direction in the back of the wave. Here we address this
problem by using microfluidics to expose cells to traveling waves of
chemoattractant with varying periods. We find that cells exhibit
cellular memory and maintain directed motion towards the wave
source in the back of the wave for the natural period of 6 minutes,
but increasingly reverse direction for longer wave periods. Further
insights into cellular memory are provided by experiments quantifying
cell motion and localization of a directional-sensing marker after
rapid gradient switches. The results can be explained by a model that
couples adaptive directional sensing to bistable cellular memory. Our
study shows how spatiotemporal cues can guide cell migration over
large distances.


Submitted by Wouter-Jan Rappel [rappel@physics.ucsd.edu]
==============================================================
[End dictyNews, volume 40, number 23]

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