Hyphal Tip-Associated Localization of Cdc42 Is F-Actin Dependent in
            <i>Candida albicans</i>

Hazan, Idit; Liu, Haoping

doi:10.1128/ec.1.6.856-864.2002

Cited by 76 publications

(80 citation statements)

References 29 publications

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“…This analogy cannot be taken too far, as proteins such as Far1p that are critical for shmoo formation in the budding yeast are not required for germ tube development in C. albicans (5). However, the ability to initiate polarized growth from a nonconstricted point of emergence, the ability to migrate the nucleus into this polarized extension, and the requirement for the actin cytoskeleton to direct the localization of the Cdc42p GTPase (52) are common characteristics of shmooing yeast cells and C. albicans cells initiating a germ tube.…”

Section: Pheromone-mediated Morphological Changesmentioning

confidence: 99%

Morphogenesis in Candida albicans

Whiteway

Bachewich²

2007

Annu. Rev. Microbiol.

362

339

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Candida albicans is termed a dimorphic fungus because it proliferates in either a yeast form or a hyphal form. The switch between these forms is the result of a complex interplay of external and internal factors and is coordinated in part by polarity-regulating proteins that are conserved among eukaryotic cells. However, yeast and hyphal cells are not the only morphological states of C. albicans. The opaque form required for mating, the pseudohyphal cell, and the chlamydospore represent distinct cell types that form in response to specific genetic or environmental conditions. In addition, hyperextended buds can form as a result of various cell cycle-related stresses. Recent studies are beginning to shed light on some of the molecular controls regulating the various morphogenetic forms of this fascinating human pathogen.

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Section: Pheromone-mediated Morphological Changesmentioning

confidence: 99%

Morphogenesis in Candida albicans

Whiteway

Bachewich²

2007

Annu. Rev. Microbiol.

362

339

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“…Conditions that disrupt proper cell cycle progression can result in polarized growth through diverse cell cycle pathways (Fig. 4) (20,33,219). Notably, depending on the phase of cell cycle arrest, the cells will have different filamentation phenotypes.…”

Section: Major Morphogenetic Signaling Cascadesmentioning

confidence: 99%

Regulatory Circuitry Governing Fungal Development, Drug Resistance, and Disease

Shapiro

Robbins

Cowen

2011

Microbiol Mol Biol Rev

499

547

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SUMMARY Pathogenic fungi have become a leading cause of human mortality due to the increasing frequency of fungal infections in immunocompromised populations and the limited armamentarium of clinically useful antifungal drugs. Candida albicans , Cryptococcus neoformans , and Aspergillus fumigatus are the leading causes of opportunistic fungal infections. In these diverse pathogenic fungi, complex signal transduction cascades are critical for sensing environmental changes and mediating appropriate cellular responses. For C. albicans , several environmental cues regulate a morphogenetic switch from yeast to filamentous growth, a reversible transition important for virulence. Many of the signaling cascades regulating morphogenesis are also required for cells to adapt and survive the cellular stresses imposed by antifungal drugs. Many of these signaling networks are conserved in C. neoformans and A. fumigatus , which undergo distinct morphogenetic programs during specific phases of their life cycles. Furthermore, the key mechanisms of fungal drug resistance, including alterations of the drug target, overexpression of drug efflux transporters, and alteration of cellular stress responses, are conserved between these species. This review focuses on the circuitry regulating fungal morphogenesis and drug resistance and the impact of these pathways on virulence. Although the three human-pathogenic fungi highlighted in this review are those most frequently encountered in the clinic, they represent a minute fraction of fungal diversity. Exploration of the conservation and divergence of core signal transduction pathways across C. albicans , C. neoformans , and A. fumigatus provides a foundation for the study of a broader diversity of pathogenic fungi and a platform for the development of new therapeutic strategies for fungal disease.

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“…Cortical actin patches are clustered at the hyphal tips during the hyphal growth phase (Wendland, 2001). In the ectomycorrhizal basidiomycete Suillus bovinus and the dimorphic fungus Candida albicans during hyphal growth stages Cdc42p was found to be localized to hyphal tips, indicating that Cdc42p is not only required for hyphal tip formation but might also play a role during polarized hyphal growth (Gorfer et al, 2001;Hazan and Liu, 2002).…”

mentioning

confidence: 99%

Apical localization of actin patches and vacuolar dynamics in Ashbya gossypii depend on the WASP homolog Wal1p

Walther

Wendland

2004

Journal of Cell Science

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Analysis of the Ashbya gossypii Wiskott-Aldrich syndrome-like gene AgWAL1 indicates that it is required for the maintenance of polarized hyphal growth. Growth and organelle dynamics of the wild type and of wal1 and other mutant strains were monitored by in vivo (fluorescence) time-lapse microscopy. Loss of WAL1 led to slow growth and defects in polarized growth that produced swellings in subapical regions, whereas formation of hyphal tips and dichotomous tip branching occurred as in the wild-type. Few actin cables in Agwal1 cells were found to insert into the hyphal tip, but specific clustering of cortical actin patches was observed in subapical regions of hyphal tips instead of at the hyphal apex. Distribution and movement of vacuoles was observed in vivo using FM4-64. In the wild type and in the slowly growing mutant strains bem2 and cla4, which lack a Rho-GTPase-activating protein and a PAK kinase, respectively, early endosomes appeared in the hyphal tip, whereas very few early endosomes and small vacuoles were found in the wal1 mutant hyphal tips, thus linking the cortical patch defect of wal1 hyphae with the distribution of endosomes. Vivid movement of vacuoles seen in the wild type and in the bem2 mutant in subapical regions was largely reduced in the wal1 and cla4 mutants. The tubular structure of mitochondria (as visualized by DIOC6 in vivo) was similar in the wild type and the wal1 mutant, although wal1 mitochondria appeared to be larger. Interestingly, mitochondria were found to insert into the hyphal tips in both strains. Our results indicate a function for Wal1p in filamentous fungi in coordinating actin patch distribution with polarized hyphal tip growth.

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Hyphal Tip-Associated Localization of Cdc42 Is F-Actin Dependent in Candida albicans

Cited by 76 publications

References 29 publications

Morphogenesis in Candida albicans

Morphogenesis in Candida albicans

Regulatory Circuitry Governing Fungal Development, Drug Resistance, and Disease

Apical localization of actin patches and vacuolar dynamics in Ashbya gossypii depend on the WASP homolog Wal1p

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