Differences in adhesion of Candida albicans 3153A cells exhibiting switch phenotypes to buccal epithelium and stratum corneum

Vargas, Kaaren; Wertz, Philip W.; Drake, David R.; Morrow, Brian J.; Soll, David R.

doi:10.1128/iai.62.4.1328-1335.1994

Cited by 42 publications

(20 citation statements)

References 28 publications

(41 reference statements)

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“…Organisms. C. albicans laboratory strains 3153A (16,17,31,32) and SC5314 (17,33), C. glabrata clinical isolate MRO-084-R (16) were used for the bulk of the studies. C. albicans clinical isolates TW 07229 and TW 072243 (34,35) were generously provided by Theodore C. White, Seattle, WA.…”

Section: Methodsmentioning

confidence: 99%

Respiratory Deficiency Enhances the Sensitivity Candida to Photodynamic Treatment

Chabrier-Roselló¹,

Foster²,

Mitra³

et al. 2008

Photochem & Photobiology

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Section: Methodsmentioning

confidence: 99%

Respiratory Deficiency Enhances the Sensitivity Candida to Photodynamic Treatment

Chabrier-Roselló¹,

Foster²,

Mitra³

et al. 2008

Photochem & Photobiology

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“…In almost every comparison, a profound difference was found. Opaque cells differed from white cells in their sensitivity to neutrophils and reactive oxygen species (Kolitila & Diamond, 1990), adhesion to human cells and plastics (Kennedy et al, 1988;Vargas et al, 1994), secretion of proteinases (Morrow et al, 1992), resistance to antifungals (Vargas et al, 2000) and susceptibility in a Drosophila phagocytosis model (Lohse & Johnson, 2008). White and opaque cells also differed in performance in a yin-yang fashion in two mouse virulence models.…”

Section: Early Ideas About the Role Of Switchingmentioning

confidence: 99%

Why doesCandida albicans switch?

Soll¹

2009

FEMS Yeast Research

123

115

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White-opaque switching in Candida albicans was first discovered in 1987. Fifteen years later, and three years after the discovery of the mating system, it was demonstrated that the switch from white to opaque was an essential step in the mating process. But this latter discovery did not reveal why C. albicans had this requirement, when Saccharomyces cerevisiae and other hemiascomycetes did not. The discovery that mating-competent opaque cells signaled mating-incompetent white cells, through the release of pheromones, to become adhesive and form biofilms provided a clue to this fundamental question. Opaque cells appeared to signal white cells to form biofilms that facilitated mating by protecting the fragile gradients of the pheromone that directed chemotropism, a process necessary for fusion. Here, we explore the discoveries and observations that have led to this hypothesis, and the ancillary questions that have risen that are related to the regulation of the unique pheromone response, the evolution of this response and the relationship between pheromone-enhanced white cell biofilms and 'asexual' biofilms formed by a/alpha cells. This discussion, therefore, focuses on a unique and complex component of the basic biology of C. albicans that relates switching, mating and pathogenesis.

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“…differentially express the drug-resistance gene CDR4, (18) opaque-phase cells differentially express the drug-resistance gene CDR3 (22) and, while white-phase cells are far more virulent than opaque-phase cells in a mouse tail injection model for systemic infections, (25) opaque-phase cells are far more proficient at colonizing mouse skin than white-phase cells. (26) White-and opaque-phase cells also differ in adhesivity, (27,28) sensitivity to white blood cells and oxidants, (29) and constraints on the bud-hypha transition. (30) When one adds up the variety of phenotypic differences between white-and opaque-phase cells, the pleiotropy proves to be truly remarkable.…”

Section: Introductionmentioning

confidence: 99%

Mating‐type locus homozygosis, phenotypic switching and mating: a unique sequence of dependencies in Candida albicans

Soll

2003

BioEssays

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A small proportion of clinical strains of Candida albicans undergo white-opaque switching. Until recently it was not clear why, since most strains carry the genes differentially expressed in the unique opaque phase. The answer to this enigma lies in the mating process. The majority of C. albicans strains are heterozygous for the mating type locus MTL (a/alpha) and cannot undergo white-opaque switching. However, when these cells undergo homozygosis at the mating type locus (i.e., become a/a or alpha/alpha), they can switch, and they must switch in order to mate. Even though the newly identified stages of mating mimic those of Saccharomyces cerevisiae, the process differs in its dependency on switching, and the effects switching has on gene regulation. This unique feature of C. albicans mating appears to be intimately intertwined with its pathogenesis. The unique, newly discovered dependencies of switching on homozygosis at the MTL locus and of mating on switching are, therefore, reviewed within the context of pathogenesis.

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Differences in adhesion of Candida albicans 3153A cells exhibiting switch phenotypes to buccal epithelium and stratum corneum

Cited by 42 publications

References 28 publications

Respiratory Deficiency Enhances the Sensitivity Candida to Photodynamic Treatment

Respiratory Deficiency Enhances the Sensitivity Candida to Photodynamic Treatment

Why doesCandida albicans switch?

Mating‐type locus homozygosis, phenotypic switching and mating: a unique sequence of dependencies in Candida albicans

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