dictyNews
Electronic Edition
Volume 39, number 24
August 23 2013
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Abstracts
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How do amoebae swim and crawl?
Jonathan D. Howe, Nicholas P. Barry, Mark S. Bretscher*
Cell Biology Division, Medical Research Council Laboratory of
Molecular Biology, Cambridge, Cambridgeshire, United Kingdom.
PLoS ONE, in press.
The surface behaviour of swimming amoebae was followed in
cells bearing a cAR1-paGFP (cyclicAMP receptor fused to a
photoactivatable-GFP) construct. Sensitized amoebae were placed
in a buoyant medium where they could swim toward a chemoattractant
cAMP source. paGFP, activated at the cell's front, remained fairly
stationary in the cell's frame as the cell advanced; the label was not
swept rearwards. Similar experiments with chemotaxing cells attached
to a substratum gave the same result. Furthermore, if the region around
a lateral projection near a crawling cell's front is marked, the projection
and the labelled cAR1 behave differently. The label spreads by diffusion
but otherwise remains stationary in the cell's frame; the lateral projection
moves rearwards on the cell (remaining stationary with respect to the
substrate), so that it ends up outside the labelled region. Furthermore,
as cAR1-GFP cells move, they occasionally do so in a remarkably
straight line; this suggests they do not need to snake to move on a
substratum. Previously, we suggested that the surface membrane of a
moving amoeba flows from front to rear as part of a polarised membrane
trafficking cycle. This could explain how swimming amoebae are able to
exert a force against the medium. Our present results indicate that, in
amoebae, the suggested surface flow does not exist: this implies that
they swim by shape changes.
Submitted by Mark Bretscher [[log in to unmask]]
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A new kind of membrane-tethered eukaryotic transcription factor that
shares an auto-proteolytic processing mechanism with bacteriophage
tail-spike proteins
Hiroshi Senoo, Tsuyoshi Araki+, Masashi Fukuzawa and Jeffrey G. Williams+*
Department of Biology, Faculty of Agriculture and Life Science, Hirosaki
University, Hirosaki, Aomori 036-8561, Japan
+ College of Life Sciences, Welcome Trust Building, University of Dundee,
Dow St., Dundee DD1 5EH UK
* corresponding author:
tel 44 1382 385823
fax 44-1382 344211
[log in to unmask]
Journal of Cell Science, in press
MrfA, a transcription factor that regulates Dictyostelium prestalk cell
differentiation, is an orthologue of the animal Myelin-gene Regulatory
Factor (MRF) proteins. We show that the MRFs contain a predicted trans-
membrane domain, suggesting that they are synthesized as membrane-
tethered proteins that are then proteolytically released. We confirm this for
MrfA but report a radically different mode of processing from that of
paradigmatic tethered transcriptional regulators; which are cleaved within
the trans-membrane domain by a dedicated protease. Instead an auto-
proteolytic cleavage mechanism, previously only described for the
intramolecular chaperone domains of bacteriophage tail-spike proteins,
processes MrfA and, by implication, the metazoan MRF proteins. We also
present evidence that the auto-proteolysis of MrfA occurs rapidly and
constitutively in the ER and that its specific role in prestalk cell differentiation
is conferred by theregulated nuclear translocation of the liberated fragment.
Submitted by Jeff Williams [[log in to unmask]]
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Iron metabolism and resistance to infection by invasive bacteria in the
social amoeba Dictyostelium discoideum
Salvatore Bozzaro*, Simona Buracco and Barbara Peracino
Department of Clinical and Biological Sciences, University of Torino,
Orbassano, Italy
Frontiers Cell Infect Microbiol, in press
Dictyostelium cells are forest soil amoebae, which feed on bacteria and
proliferate as solitary cells until bacteria are consumed. Starvation triggers a
change in life style, forcing cells to gather into aggregates to form multicellular
organisms capable of cell differentiation and morphogenesis. As a soil amoeba
and a phagocyte that grazes on bacteria as the obligate source of food,
Dictyostelium could be a natural host of pathogenic bacteria. Indeed, many
pathogens that occasionally infect humans are hosted for most of their time in
protozoa or free-living amoebae, where evolution of their virulence traits occurs.
Due to these features and its amenability to genetic manipulation, Dictyostelium
has become a valuable model organism for studying strategies of both the host
to resist infection and the pathogen to escape the defence mechanisms.
Similarly to higher eukaryotes, iron homeostasis is crucial for Dictyostelium
resistance to invasive bacteria. Iron is essential for Dictyostelium, as both iron
deficiency or overload inhibit cell growth. The Dictyostelium genome shares
with mammals many genes regulating iron homeostasis. Iron transporters of
the Nramp (Slc11A) family are represented with two genes, encoding Nramp1
and Nramp2. Like the mammalian ortholog, Nramp1 is recruited to phagosomes
and macropinosomes, whereas Nramp2 is a membrane protein of the contractile
vacuole network, which regulates osmolarity. Nramp1 and Nramp2 localization
in distinct compartments suggests that both proteins synergistically regulate iron
homeostasis. Rather than by absorption via membrane transporters, iron is
likely gained by degradation of ingested bacteria and efflux via Nramp1 from
phagosomes to the cytosol. Nramp gene disruption increases Dictyostelium
sensitivity to infection, enhancing intracellular growth of Legionella or
Mycobacteria. Generation of mutants in other "iron genes" will help identify
genes essential for iron homeostasis and resistance to pathogens.
Submitted by Salvatore Bozzaro [[log in to unmask]]
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[End dictyNews, volume 39, number 24]
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