dictyNews
Electronic Edition
Volume 44, number 8
March 16, 2018
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Abstracts
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Calcineurin silencing in Dictyostelium discoideum leads to cellular
alterations affecting mitochondria, gene expression, and oxidative
stress response.
Konstanze Kobel-Höller; Kevin Gley; Janina Jochinke; Kristina Heider;
Verena Nadin Fritsch; Ha Viet Duc Nguyen; Renate Radek; Ria
Baumgrass; Rupert Mutzel; Sascha Thewes
Protist, in press
Calcineurin is involved in development and cell differentiation of the social
amoeba Dictyostelium discoideum. However, since knockouts of the
calcineurin-encoding genes are not possible in D. discoideum it is
assumed that the phosphatase also plays a crucial role during vegetative
growth of the amoebae. Therefore, we investigated the role of calcineurin
during vegetative growth in D. discoideum. RNAi-silenced calcineurin
mutants showed cellular alterations with an abnormal morphology of
mitochondria and had increased content of mitochondrial DNA (mtDNA).
In contrast, mitochondria showed no substantial functional impairment.
Calcineurin-silencing led to altered expression of calcium-regulated genes
as well as mitochondrially encoded genes. Furthermore, genes related to
oxidative stress were higher expressed in the mutants, which correlated to
an increased resistance towards reactive oxygen species (ROS). Most of
the changes observed during vegetative growth were not seen after
starvation of the calcineurin mutants. We show that impairment of calcineurin
led to many subtle, but in the sum crucial cellular alterations in vegetative
D. discoideum cells. As these alterations were not observed after starvation
we propose a dual role for calcineurin during growth and development. Our
results imply that calcineurin is one player in the mutual interplay between
mitochondria and ROS during vegetative growth.
submitted by: Sascha Thewes [[log in to unmask]]
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Collective regulation of cell motility using an accurate density-sensing system
Joseph d’Alessandro1,†, Lauriane Mas2, Laurence Aubry2, Jean-Paul Rieu1,
Charlotte Rivière1 and Christophe Anjard1
1University Lyon, Université Claude Bernard Lyon 1, CNRS, Institut Lumière
Matière, 69622, Villeurbanne, France
2University Grenoble Alpes, CEA, Inserm, BIG-BGE, 38000 Grenoble, France
journal of the Royal Society Interface , in press
The capacity of living cells to sense their population density and to migrate
accordingly is essential for the regulation of many physiological processes.
However, the mechanisms used to achieve such functions are poorly known.
Here, based on the analysis of multiple trajectories of vegetative Dictyostelium
discoideum cells, we investigate such a system extensively. We show that the
cells secrete a high-molecular-weight quorum-sensing factor (QSF) in their
medium. This extracellular signal induces, in turn, a reduction of the cell
movements, in particular, through the downregulation of a mode of motility
with high persistence time. This response appears independent of cAMP and
involves a G-protein-dependent pathway. Using a mathematical analysis of
the cells’ response function, we evidence a negative feedback on the QSF
secretion, which unveils a powerful generic mechanism for the cells to detect
when they exceed a density threshold. Altogether, our results provide a
comprehensive and dynamical view of this system enabling cells in a
scattered population to adapt their motion to their neighbours without
physical contact.
submitted by: Christophe Anjard [[log in to unmask]]
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Dictyostelium Erk2 is an Atypical MAPK Required for Chemotaxis
David J. Schwebs1,3, Miao Pan2, Nirakar Adhikari1, Nick A. Kuburich1,
Tian Jin2, and Jeffrey A. Hadwiger1*
Cellular Signalling, in press
The Dictyostelium genome encodes only two MAPKs, Erk1 and Erk2, and
both are expressed during growth and development. Reduced levels of Erk2
expression have been shown previously to restrict cAMP production during
development but still allow for chemotactic movement. In this study the erk2
gene was disrupted to eliminate Erk2 function. The absence of Erk2 resulted
in a complete loss of folate and cAMP chemotaxis suggesting that this MAPK
plays an integral role in the signaling mechanisms involved with this cellular
response. However, folate stimulation of early chemotactic responses, such
as Ras and PI3K activation and rapid actin filament formation, were not
affected by the loss of Erk2 function. The erk2- cells had a severe defect in
growth on bacterial lawns but assays of bacterial cell engulfment displayed
only subtle changes in the rate of bacterial engulfment. Only cells with no
MAPK function, erk1-erk2- double mutants, displayed a severe proliferation
defect in axenic medium. Loss of Erk2 impaired the phosphorylation of Erk1
in secondary responses to folate stimulation indicating that Erk2 has a role in
the regulation of Erk1 activation during chemotaxis. Loss of the only known
Dictyostelium MAPK kinase, MekA, prevented the phosphorylation of Erk1 but
not Erk2 in response to folate and cAMP confirming that Erk2 is not regulated
by a conventional MAP2K. This lack of MAP2K phosphorylation of Erk2 and the
sequence similarity of Erk2 to mammalian MAPK15 (Erk8) suggest that the
Dictyostelium Erk2 belongs to a group of atypical MAPKs. MAPK activation has
been observed in chemotactic responses in a wide range of organisms but this
study demonstrates an essential role for MAPK function in chemotactic
movement. This study also confirms that MAPKs provide critical contributions
to cell proliferation.
submitted by: Jeff Hadwiger [[log in to unmask]]
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[End dictyNews, volume 44, number 8]
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