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pubmed-article:20384695pubmed:abstractTextGrowth of cells in contact with an abiotic or biological surface profoundly affects cellular physiology. In the opportunistic human pathogen, Candida albicans, growth on a semi-solid matrix such as agar results in invasive filamentation, a process in which cells change their morphology to highly elongated filamentous hyphae that grow into the matrix. We hypothesized that a plasma membrane receptor-type protein would sense the presence of matrix and activate a signal transduction cascade, thus promoting invasive filamentation. In this communication, we demonstrate that during growth in contact with a semi-solid surface, activation of a MAP kinase, Cek1p, is promoted, in part, by a plasma membrane protein termed Dfi1p and results in invasive filamentation. A C. albicans mutant lacking Dfi1p showed reduced virulence in a murine model of disseminated candidiasis. Dfi1p is a relatively small, integral membrane protein that localizes to the plasma membrane. Some Dfi1p molecules become cross-linked to the carbohydrate polymers of the cell wall. Thus, Dfi1p is capable of linking the cell wall to the plasma membrane and cytoplasm.lld:pubmed
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pubmed-article:20384695pubmed:dateRevised2011-9-26lld:pubmed
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pubmed-article:20384695pubmed:articleTitleA Candida albicans cell wall-linked protein promotes invasive filamentation into semi-solid medium.lld:pubmed
pubmed-article:20384695pubmed:affiliationDepartment of Molecular Biology and Microbiology, Tufts University, Boston, MA 02111, USA.lld:pubmed
pubmed-article:20384695pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20384695pubmed:publicationTypeResearch Support, U.S. Gov't, Non-P.H.S.lld:pubmed
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