Physiological adventures in : farnesol and ubiquinones.

SUMMARYFarnesol was first identified as a quorum-sensing molecule, which blocked the yeast to hyphal transition in , 22 years ago. However, its interactions with biology are surprisingly complex. Exogenous (secreted or supplied) farnesol can also act as a virulence factor during pathogenesis and as a fungicidal agent triggering apoptosis in other competing fungi.

Longer Ubiquinone Side Chains Contribute to Enhanced Farnesol Resistance in Yeasts.

Ubiquinones (UQ) are intrinsic lipid components of many membranes. Besides their role in electron-transfer reactions there is evidence for them acting as free radical scavengers, yet their other roles in biological systems have received little study. The dimorphic fungal pathogen secretes farnesol as both a virulence factor and a quorum-sensing molecule.

Sho1p Connects Glycolysis to Ras1-cAMP Signaling and Is Required for Microcolony Formation in Candida albicans.

is an opportunistic, dimorphic fungus that causes candidiasis in immunocompromised people. forms specialized structures called microcolonies that are important for surface adhesion and virulence. Microcolonies form in response to specific environmental conditions and require glycolytic substrates for optimal growth.

biofilm development is governed by cooperative attachment and adhesion maintenance proteins.

The opportunistic fungal pathogen is capable of adhering to the oral mucosa despite forces created by salivary flow. Although many fungal adhesion proteins have been identified, less is known about the temporal development of cell adhesion and biofilm growth in a flow environment. In this study, we use a flow system with real-time imaging of cells as they adhere and grow.

Filamentous Non- Species Adhere to and Benefit From Dual Biofilm Growth.

Non- species (NACS) are often isolated along with in cases of oropharyngeal candidiasis. readily forms biofilms in conjunction with other oral microbiota including both bacteria and yeast. Adhesion between species is important to the establishment of these mixed biofilms, but interactions between and many NACS are not well-characterized.

Candida albicans Ras1 Inactivation Increases Resistance to Phagosomal Killing by Human Neutrophils.

Host phagocytic cells are crucial players in initial defense against infection. utilizes MAP kinases and Ras1 stress response signaling pathways to protect itself from killing by immune cells. In this study, we tested the importance of these pathways in phagocytosis by neutrophils and subsequent phagosomal survival.

Fluconazole-Resistant Candida auris Is Susceptible to Salivary Histatin 5 Killing and to Intrinsic Host Defenses.

is a newly identified species causing invasive candidemia and candidiasis. It has broad multidrug resistance (MDR) not observed for other pathogenic species. Histatin 5 (Hst 5) is a well-studied salivary cationic peptide with significant antifungal activity against and is an attractive candidate for treating MDR fungi, since antimicrobial peptides induce minimal drug resistance.

Candida albicans ISW2 Regulates Chlamydospore Suspensor Cell Formation and Virulence In Vivo in a Mouse Model of Disseminated Candidiasis.

Formation of chlamydospores by Candida albicans was an established medical diagnostic test to confirm candidiasis before the molecular era. However, the functional role and pathological relevance of this in vitro morphological transition to pathogenesis in vivo remain unclear. We compared the physical properties of in vitro-induced chlamydospores with those of large C.

Biotin Auxotrophy and Biotin Enhanced Germ Tube Formation in Candida albicans.

Due to the increased number of immunocompromised patients, infections with the pathogen Candida albicans have significantly increased in recent years. C. albicans transition from yeast to germ tubes is one of the essential factors for virulence.