dictyNews
Electronic Edition
Volume 44, number 10
April 6, 2018
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Abstracts
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Analysis of Random Migration of Dictyostelium Amoeba in Confined
and Unconfined Environments
Litschko C, Damiano-Guercio J, Brühmann S, Faix J.
Methods Mol Biol. 2018;1749:341-350.
Dictyostelium discoideum has proven to be an excellent model to
study amoeboid cell migration. During their life cycle, Dictyostelium
cells exhibit distinct modes of motility. Individual growth-phase cells
explore new territories by random cell migration using the core cell
motility machinery, but they can also hunt bacteria by detection and
chemotaxis toward the by-product folate. After depletion of nutrients,
the cells initiate a developmental program allowing streaming of the
cells into aggregation centers by chemotaxis toward cAMP and by
cell-to-cell adhesion. Subsequent development is associated with
complex rotational movement of the compacted aggregates to drive
cell type specific sorting, which in turn is necessary for terminal
culmination and formation of fruiting bodies. Here we describe a
protocol for the analyses of cell motility of vegetative Dictyostelium
cells in unconfined and mechanically confined settings.
submitted by: Jan Faix [[log in to unmask]]
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IreA controls endoplasmic reticulum stress-induced autophagy and
survival through homeostasis recovery
Eunice Domínguez-Martín, Laura Ongay-Larios, Laura Kawasaki,
Olivier Vincent, Gerardo Coello, Roberto Coria and Ricardo Escalante
Mol. Cell. Biol., in press
The Unfolded Protein Response (UPR) is an adaptive pathway that
restores cellular homeostasis after endoplasmic reticulum (ER) stress.
The ER-resident kinase/ribonuclease Ire1 is the only UPR sensor
conserved during evolution. Autophagy, a lysosomal degradative
pathway, also contributes to the recovery of cell homeostasis after
ER-stress but the interplay between these two pathways is still poorly
understood. We describe the Dictyostelium discoideum ER-stress
response and characterize its single bonafide Ire1 orthologue, IreA.
We found that tunicamycin (TN) triggers a gene-expression
reprogramming that increases the protein folding capacity of the ER
and alleviates ER protein load. Further, IreA is required for cell-survival
after TN-induced ER-stress and is responsible for nearly 40% of the
transcriptional changes induced by TN. The response of Dictyostelium
cells to ER-stress involves the combined activation of an IreA-
dependent gene expression program and the autophagy pathway.
These two pathways are independently activated in response to
ER-stress but, interestingly, autophagy requires IreA at a later stage
for proper autophagosome formation. We propose that unresolved
ER-stress in cells lacking IreA causes structural alterations of the ER,
leading to a late-stage blockade of autophagy clearance. This
unexpected functional link may critically affect eukaryotic cell survival
under ER-stress.
submitted by: Ricardo Escalante [[log in to unmask]]
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