Cornet, Muriel;
Bidard, Frédérique;
Schwarz, Patrick;
Da Costa, Grégory;
Blanchin-Roland, Sylvie;
Dromer, Françoise;
Gaillardin, Claude
Deletions of Endocytic Components VPS28 and VPS32 Affect Growth at Alkaline pH and Virulence through both RIM101 -Dependent and RIM101 -Independent Pathways in Candida albicans
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Medientyp:
E-Artikel
Titel:
Deletions of Endocytic Components VPS28 and VPS32 Affect Growth at Alkaline pH and Virulence through both RIM101 -Dependent and RIM101 -Independent Pathways in Candida albicans
Beteiligte:
Cornet, Muriel;
Bidard, Frédérique;
Schwarz, Patrick;
Da Costa, Grégory;
Blanchin-Roland, Sylvie;
Dromer, Françoise;
Gaillardin, Claude
Erschienen:
American Society for Microbiology, 2005
Beschreibung:
<jats:title>ABSTRACT</jats:title>
<jats:p>
Ambient pH signaling involves a cascade of conserved Rim or Pal products in ascomycetous yeasts or filamentous fungi, respectively. Recent evidences in the fungi
<jats:italic>Aspergillus nidulans</jats:italic>
,
<jats:italic>Saccharomyces cerevisiae</jats:italic>
,
<jats:italic>Yarrowia lipolytica</jats:italic>
, and
<jats:italic>Candida albicans</jats:italic>
suggested that components of endosomal sorting complexes required for transport (ESCRT) involved in endocytic trafficking were needed for signal transduction along the Rim pathway. In this study, we confirm these findings with
<jats:italic>C. albicans</jats:italic>
and show that Vps28p (ESCRT-I) and Vps32p/Snf7p (ESCRT-III) are required for the transcriptional regulation of known targets of the Rim pathway, such as the
<jats:italic>PHR1</jats:italic>
and
<jats:italic>PHR2</jats:italic>
genes encoding cell surface proteins, which are expressed at alkaline and acidic pH, respectively. We additionally show that deletion of these two
<jats:italic>VPS</jats:italic>
genes, particularly
<jats:italic>VPS32</jats:italic>
, has a more drastic effect than a
<jats:italic>RIM101</jats:italic>
deletion on growth at alkaline pH and that this effect is only partially suppressed by expression of a constitutively active form of Rim101p. Finally, in an in vivo mouse model, both
<jats:italic>vps</jats:italic>
null mutants were significantly less virulent than a
<jats:italic>rim101</jats:italic>
mutant, suggesting that
<jats:italic>VPS28</jats:italic>
and
<jats:italic>VPS32</jats:italic>
gene products affect virulence both through Rim-dependent and Rim-independent pathways.
</jats:p>