dictyNews Volume 32 Number 13

Published in

· 10 months ago

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. 

========= 
Abstracts 
========= 

 

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]