Effects of neutrophils and in vitro oxidants on survival and phenotypic switching of Candida albicans WO-1

Kolotila, Michael P.; Diamond, Richard D.

doi:10.1128/iai.58.5.1174-1179.1990

Cited by 111 publications

(36 citation statements)

References 29 publications

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“…1a) Slutsky et al, 1987). Early studies revealed variable rates of switching (Rikkerink et al, 1988;Bergen et al, 1990;Soll et al, 1991), no doubt because a variety of environmental conditions affected it (Rikkerink et al, 1988;Morrow et al, 1989;Kolitila & Diamond, 1990;Dumitru et al, 2007;Ramirez-Zavala et al, 2008;Huang et al, 2009). Single cell studies indicated that in vitro at 25 1C, opaque cells immediately gave rise to white cells, but white cells formed a pseudohyphal intermediate, which in turn gave rise to opaque cells (Bergen et al, 1990) (Fig.…”

Section: Phenotypic Complexitymentioning

confidence: 97%

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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Section: Phenotypic Complexitymentioning

confidence: 97%

Why doesCandida albicans switch?

Soll¹

2009

FEMS Yeast Research

123

115

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“…Although switching is stochastic, environmental cues can affect the frequency of switching events in one direction or the other. These cues include temperature (Rikkerink et al, 1988), oxidative stress (Kolotila and Diamond, 1990), anaerobic conditions (Dumitru et al, 2007;Ramírez-Zavala et al, 2008) and carbon dioxide (Huang et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Temporal anatomy of an epigenetic switch in cell programming: the white‐opaque transition of C. albicans

Lohse

Johnson

2010

Molecular Microbiology

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SummaryThe human pathogen Candida albicans undergoes a well-defined switch between two distinct cell types, named 'white' and 'opaque'. White and opaque cells differ in metabolic preferences, mating behaviours, cellular morphologies and host interactions. Each cell type is stable through many generations; switching between them is rare, stochastic and occurs without any known changes in the primary sequence of the genome; thus the switch is epigenetic. The whiteopaque switch is regulated by a transcriptional circuit, composed of four regulators arranged in a series of interlocking feedback loops. To understand how switching occurs, we investigated the order of regulatory changes that occur during the switch from the opaque to the white cell type. Surprisingly, changes in key transcriptional regulators occur gradually, extending over several cell divisions with little cell-to-cell variation. Additional experiments, including perturbations to regulator concentrations, refine the signature of the commitment point. Transcriptome analysis reveals that opaque cells begin to globally resemble white cells well before they irreversibly commit to switching. We propose that these characteristics of the switching process permit C. albicans to 'test the waters' before making an all-ornone decision.

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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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Effects of neutrophils and in vitro oxidants on survival and phenotypic switching of Candida albicans WO-1

Cited by 111 publications

References 29 publications

Why doesCandida albicans switch?

Why doesCandida albicans switch?

Temporal anatomy of an epigenetic switch in cell programming: the white‐opaque transition of C. albicans

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

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