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dictyNews Volume 43 Number 07

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Published in 
Dicty News
 · 11 months ago

dictyNews 
Electronic Edition
Volume 43, number 7
April 7, 2017

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
=========


Does high relatedness promote cheater-free multicellularity in synthetic lifecycles?

R. F. Inglis, E. Ryu, O. Asikhia, J. E. Strassmann & D. C. Queller


Journal of Evolutionary Biology, in press

The evolution of multicellularity is one of the key transitions in evolution and
requires extreme levels of cooperation between cells. However, even when cells
are genetically identical, noncooperative cheating mutants can arise that cause
a breakdown in cooperation. How then, do multicellular organisms maintain
cooperation between cells? A number of mechanisms that increase relatedness
amongst cooperative cells have been implicated in the maintenance of cooperative
multicellularity including single-cell bottle- necks and kin recognition. In this study,
we explore how relatively simple biological processes such as growth and dispersal
can act to increase related-ness and promote multicellular cooperation. Using
experimental populations of pseudo- organisms, we found that manipulating growth
and dispersal of clones of a social amoeba to create high levels of relatedness was
sufficient to prevent the spread of cheating mutants. By contrast, cheaters were able
to spread under low-relatedness conditions. Most surprisingly, we saw the largest
increase in cheating mutants under an experimental treatment that should create
intermediate levels of relatedness. This is because one of the factors raising
relatedness, structured growth, also causes high vulnerability to growth rate cheaters.


submitted by: Fredrik Inglis [inglis@wustl.edu]
———————————————————————————————————————


Evidence that differentiation-inducing factor-1 controls chemotaxis and cell
differentiation, at least in part, via mitochondria in Dictyostelium discoideum.

Yuzuru Kubohara*, Haruhisa Kikuchi, Van Hai Nguyen, Hidekazu Kuwayama,
and Yoshiteru Oshima

*Laboratory of Health and Life Science, Graduate School of Health and Sports
Science, Juntendo University, Inzai, Chiba 270-1695, Japan


Biology Open, in press

Differentiation-inducing factor-1 (DIF-1) is an important regulator of cell
differentiation and chemotaxis in the development of the cellular slime mold
Dictyostelium discoideum. However, the entire signaling pathways downstream
of DIF-1 remain to be elucidated. To characterize DIF-1 and its potential
receptor(s), we synthesized two fluorescent derivatives of DIF-1, DIF-1-BODIPY
and DIF-1-NBD, and investigated their biological activities and cellular localization.
DIF-1-BODIPY (5 microM) and DIF-1 (2 nM) induced stalk cell differentiation in
the DIF-deficient strain HM44 in the presence of cAMP, whereas DIF-1-NBD
(5 microM) had no effect. Microscopic analyses revealed that the biologically
active derivative, DIF-1-BODIPY, was incorporated by stalk cells at late stages of
differentiation and was localized to mitochondria. The mitochondrial uncouplers
CCCP (carbonyl cyanide m-chlorophenylhydrazone) at 25–50 nM and DNP
(dinitrophenol) at 2.5–5 microM induced partial stalk cell differentiation in HM44 in
the presence of cAMP. DIF-1-BODIPY (1–2 microM) and DIF-1 (10 nM), as well
as CCCP and DNP, suppressed chemotaxis in the wild-type strain Ax2 in shallow
cAMP gradients. These results suggest that DIF-1-BODIPY and DIF-1 induce stalk
cell differentiation and modulate chemotaxis, at least in part, by disturbing
mitochondrial activity.


submitted by: Yuzuru Kubohara [ykuboha@juntendo.ac.jp]
———————————————————————————————————————


Production of Novel Bispyrone Metabolites in the Cellular Slime Mold Dictyostelium
giganteum Induced by Zinc(II) Ion

Van Hai Nguyen, Haruhisa Kikuchi, Hikaru Sasaki, Kyoichi Iizumi, Yuzuru Kubohara,
Yoshiteru Oshima.


Tetrahedron 2017, 73, 583-588; http://doi.org/10.1016/j.tet.2016.12.040

In this study, Zn2+ induced the production of two new bispyrone-type metabolites,
dictyobispyrone B and E, in the cellular slime mold Dictyostelium giganteum. Their
structures were proposed on the basis of spectroscopic analysis and confirmed by
chemical synthesis. They possess a novel alpha,alpha-bispyrone skeleton modified
with long carbon chains. Both could be formed from two different polyketide chains
through a novel biosynthetic pathway. Our results indicate that cultivation of cellular
slime molds in the presence of Zn2+ is a useful technique for discovering other
structurally unique compounds.


submitted by: Haruhisa Kikuchi [hal@mail.pharm.tohoku.ac.jp]
———————————————————————————————————————


TRE5-A retrotransposition profiling reveals putative RNA polymerase III transcription
complex binding sites on the Dictyostelium extrachromosomal rDNA element

Thomas Spaller1, Marco Groth2, Gernot Glöckner3, Thomas Winckler1

1 Pharmaceutical Biology, Institute of Pharmacy, University of Jena, Germany
2 Core Facility DNA Sequencing, Leibniz Institute for Age Research – Fritz Lipmann
Institute, Jena, Germany
3 Institute for Biochemistry I, Medical Faculty, University of Cologne, Germany


PLOS ONE, accepted

The amoeba Dictyostelium discoideum has a haploid genome in which two thirds of
the DNA encodes proteins. Consequently, the space available for selfish mobile
elements to expand without excess damage to the host genome is limited. The non-
long terminal repeat retrotransposon TRE5-A maintains an active population in the
D. discoideum genome and apparently adapted to this gene-dense environment by
targeting positions ~47 bp upstream of tRNA genes that are devoid of protein-coding
regions. Because only ~24% of tRNA genes are associated with a TRE5-A element
in the reference genome, we evaluated whether TRE5-A retrotransposition is limited
to this subset of tRNA genes. We determined that a tagged TRE5-A element
(TRE5-Absr) integrated at 384 of 405 tRNA genes, suggesting that expansion of the
current natural TRE5-A population is not limited by the availability of targets. We
further observed that TRE5-Absr targets the ribosomal 5S gene on the multicopy
extrachromosomal DNA element that carries the ribosomal RNA genes, indicating
that TRE5-A integration may extend to the entire RNA polymerase III (Pol III)
transcriptome. We determined that both natural TRE5-A and cloned TRE5-Absr
retrotranspose to locations on the extrachromosomal rDNA element that contain tRNA
gene-typical A/B box promoter motifs without displaying any other tRNA gene context.
Based on previous data suggesting that TRE5-A targets tRNA genes by locating
Pol III transcription complexes, we propose that A/B box loci reflect Pol III transcription
complex assembly sites that possess a function in the biology of the
extrachromosomal rDNA element.


submitted by: Thomas Winckler [t.winckler@uni-jena.de]
———————————————————————————————————————


Regulation of nucleosome positioning by a CHD Type III chromatin remodeler and
its relationship to developmental gene expression in Dictyostelium.

James L. Platt, Nicholas A. Kent, Alan R. Kimmel and Adrian J. Harwood (2017)


Genome Research 27: 591-600; http://genome.cshlp.org/content/27/4/591.full

Nucleosome placement and repositioning can direct transcription of individual genes;
however, the precise interactions of these events are complex and largely unresolved
at the whole-genome level. The Chromodomain-Helicase-DNA binding (CHD) Type III
proteins are a subfamily of SWI2/SNF2 proteins that control nucleosome positioning
and are associated with several complex human disorders, including CHARGE
syndrome and autism. Type III CHDs are required for multicellular development of
animals and Dictyostelium but are absent in plants and yeast. These CHDs can mediate
nucleosome translocation in vitro, but their in vivo mechanism is unknown. Here, we use
genome-wide analysis of nucleosome positioning and transcription profiling to investigate
the in vivo relationship between nucleosome positioning and gene expression during
development of wild-type (WT) Dictyostelium and mutant cells lacking ChdC, a Type III
CHD protein ortholog. We demonstrate major nucleosome positional changes associated
with developmental gene regulation in WT. Loss of chdC caused an increase of intragenic
nucleosome spacing and misregulation of gene expression, affecting ~50% of the genes
that are repositioned during WT development. These analyses demonstrate active
nucleosome repositioning during Dictyostelium multicellular development, establish an in
vivo function of CHD Type III chromatin remodeling proteins in this process, and reveal
the detailed relationship between nucleosome positioning and gene regulation, as cells
transition between developmental states.


submitted by: Adrian Harwood [harwoodaj@cf.ac.uk]
==============================================================
[End dictyNews, volume 43, number 7]

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