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      • Involvement of a Quorum-Sensing-Regulated Lipase Secreted by a Clinical Isolate of Burkholderia glumae in Severe Disease Symptoms in Rice

        Devescovi, Giulia,Bigirimana, Joseph,Degrassi, Giuliano,Cabrio, Laura,LiPuma, John J.,Kim, Jinwoo,Hwang, Ingyu,Venturi, Vittorio American Society for Microbiology 2007 Applied and environmental microbiology Vol.73 No.15

        <B>ABSTRACT</B><P><I>Burkholderia glumae</I> is an emerging rice pathogen in several areas around the world. Closely related <I>Burkholderia</I> species are important opportunistic human pathogens for specific groups of patients, such as patients with cystic fibrosis and patients with chronic granulomatous disease. Here we report that the first clinical isolate of <I>B. glumae</I>, strain AU6208, has retained its capability to be very pathogenic to rice. As previously reported for rice isolate <I>B. glumae</I> BGR1 (and also for the clinical isolate AU6208), TofI or TofR acyl homoserine lactone (AHL) quorum sensing played a pivotal role in rice virulence. We report that AHL quorum sensing in <I>B. glumae</I> AU6208 regulates secreted LipA lipase and toxoflavin, the phytotoxin produced by <I>B. glumae. B. glumae</I> AU6208 <I>lipA</I> mutants were no longer pathogenic to rice, indicating that the lipase is an important virulence factor. It was also established that type strain <I>B. glumae</I> ATCC 33617 did not produce toxoflavin and lipase and was nonpathogenic to rice. It was determined that in strain ATCC 33617 the LuxR family quorum-sensing sensor/regulator TofR was inactive. Introducing the <I>tofR</I> gene of <I>B. glumae</I> AU6208 in strain ATCC 33617 restored its ability to produce toxoflavin and the LipA lipase. This study extends the role of AHL quorum sensing in rice pathogenicity through the regulation of a lipase which was demonstrated to be a virulence factor. It is the first report of a clinical <I>B. glumae</I> isolate retaining strong rice pathogenicity and finally determined that <I>B. glumae</I> can undergo phenotypic conversion through a spontaneous mutation in the <I>tofR</I> regulator.</P>

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