dictyNews
Electronic Edition
Volume 32, number 13
May 15, 2009

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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 AMPK α subunit. Conversely,  
mitochondrial
dysfunction is phenocopied and intracellular Legionella growth enhanced,
by overexpressing an active form of AMPKα 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 [[log in to unmask]]
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[End dictyNews, volume 32, number 13]