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dictyNews Volume 32 Number 13
dictyNews
Electronic Edition
Volume 32, number 13
May 15, 2009
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.
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Abstracts
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Legionella pneumophila multiplication is enhanced by chronic AMPK signalling in
mitochondrially diseased Dictyostelium cells.
Lisa Francione1, Paige K. Smith1, Sandra L. Accari1, Philip E. Taylor2,
Paul B. Bokko1, Salvatore Bozzaro3, Peter L. Beech2 and Paul R. Fisher1*.
1 Department of Microbiology, La Trobe University, VIC 3086, Australia
2 Centre for Cellular and Molecular Biology, Deakin University, Burwood,
VIC 3125, Australia
3 Department of Clinical and Biological Sciences, University of Turin,
Ospedale S. Luigi, 10043 Orbassano, Italy
Disease Models and Mechanisms, in press
Human patients with mitochondrial diseases are more susceptible to bacterial
infections, particularly of the respiratory tract. To investigate the
susceptibility of mitochondrially diseased cells to an intracellular
bacterial respiratory pathogen, we exploited the advantages of Dictyostelium
discoideum as an established model for mitochondrial disease and for
Legionella pneumophila pathogenesis. Legionella infection of macrophages
involves recruitment of mitochondria to the Legionella-containing phagosome.
We confirm here that this also occurs in Dictyostelium and investigate the
effect of mitochondrial dysfunction on host cell susceptibility to Legionella.
In mitochondrially diseased Dictyostelium strains, the pathogen was taken
up at normal rates, but it grew faster and reached counts that were twofold
higher than in the wild type host. We previously reported that other
mitochondrial disease phenotypes for Dictyostelium are due to activity
of an energy-sensing cellular alarm protein, AMP-activated protein kinase
(AMPK). Here we show that the increased ability of mitochondrially diseased
cells to support Legionella proliferation is suppressed by antisense-inhibiting
expression of the catalytic AMPKalpha subunit. Conversely, mitochondrial
dysfunction is phenocopied and intracellular Legionella growth enhanced,
by overexpressing an active form of AMPKalpha in otherwise normal cells.
These results indicate that AMPK signalling in response to mitochondrial
dysfunction enhances Legionella proliferation in host cells.
Submitted by: Paul Fisher [P.Fisher@latrobe.edu.au]
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[End dictyNews, volume 32, number 13]
