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Candida Infection Biology – fungal armoury, battlefields ... - FINSysB

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Poster number: 24<br />

Characterization of the <strong>Candida</strong> albicans PKH1 and YPK1<br />

genes for their roles in biofilm formation and cell wall<br />

integrity<br />

Vitor Cabral 1,2 , Arnaud Firon 1,2 , Tobias Schwarzmüller 3 , Karl Kuchler 3 ,<br />

Christophe d’Enfert 1,2 and Sophie Bachellier-Bassi 1,2<br />

1 Institut Pasteur, Unité Biologie et Pathogénicité Fongiques, Département Génomes et<br />

Génétique, F-75015 Paris, France; 2 INRA, USC2019, F-75015 Paris, France; 3 Medical<br />

University Vienna, Max F. Perutz Laboratories, Christian Doppler Laboratory for <strong>Infection</strong><br />

<strong>Biology</strong>, Department of Medical Biochemistry, A-1030 Vienna, Austria<br />

In Saccharomyces cerevisiae, the Pkh1/Pkh2 and Ypk1/Ypk2 protein kinases are<br />

part of a signaling cascade important for maintenance of cell wall integrity. Our<br />

analysis of a large collection of <strong>Candida</strong> glabrata knock-out mutants for their ability<br />

to form biofilms has revealed that the C. glabrata Pkh2 protein kinase<br />

(CAGL0I07513g) is necessary for growth on solid surfaces and efficient biofilm<br />

formation while Pkh1/CAGL0G04609g is not (Schwarzmüller et al., in preparation).<br />

<strong>Candida</strong> albicans has only one gene for the Pkh protein kinase and one gene for<br />

the Ypk protein kinase that we have named PKH1 and YPK1, respectively. In order<br />

to test whether the Pkh1 and Ypk1 protein kinases also play a role in biofilm<br />

formation in C. albicans, heterozygous and homozygous knockout mutants for the<br />

YPK1 and PKH1 genes have been constructed. Preliminary data show that the<br />

ypk1∆/ypk1∆ knock-out mutant has altered sensitivity to the cell wall perturbing<br />

agents Congo Red and Calcofluor White suggesting that Ypk1 might perform a<br />

function similar to that of Ypk1 and Ypk2 in S. cerevisiae. Additional studies of these<br />

mutants and complemented strains are ongoing and will be presented.<br />

We are grateful to the European Commission for funding the <strong>FINSysB</strong> Marie Curie Initial Training Network<br />

(PITN-GA-2008-214004).<br />

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