The Effects of Carbonate on Candida albicans Filamentation, Biofilm Formation, and Antifungal Resistance.

Candida albicans, a member of the normal microbial population of healthy humans, is an opportunistic pathogen that can cause serious disease in immunocompromised patients. An important virulence factor of C. albicans is the formation of biofilms.

Constitutive ALS3 expression in Candida albicans enhances adhesion and biofilm formation of efg1, but not cph1 mutant strains.

Adhesion to living and non-living surfaces is an important virulence trait of the fungal pathogen Candida albicans. Biofilm formation in this organism depends on the expression of a number of cell surface proteins including the hypha-specific protein Als3p. Loss of ALS3 impairs biofilm formation and decreases cell-cell adhesion.

Examining the effects of BRG1 over-expression on Candida albicans strains growing as pseudohyphae.

The pathogen Candida albicans is pleiomorphic and grows in yeast and filamentous forms but the relationship between the regulation of different filamentous forms is unclear. BRG1 encodes a DNA binding protein which is an important regulator of morphology. Mutants lacking BRG1 grow as yeast under all conditions tested and over-expressing BRG1 drives hyphal growth even in the absence of inducing signals.

Anaerobic conditions are a major influence on Candida albicans chlamydospore formation.

Candidiasis now represents the fourth most frequent nosocomial infection both in the USA and worldwide. Candida albicans is an increasingly common threat to human health as a consequence of AIDS, steroid therapy, organ and tissue transplantation, cancer therapy, broad-spectrum antibiotics, and other immune defects. Unfortunately, these infections carry unacceptably high morbidity, mortality rates and important economic repercussions (estimated total direct cost of approximately 2 billion dollars in 1998 in US hospitals alone).

Geldanamycin-Induced Morphological Changes Require Candida albicans Hyphal Growth Regulatory Machinery.

In Candida albicans, geldanamycin treatment inhibits the essential chaperone Hsp90 and induces a change from yeast to filamentous morphology, likely by impeding cell cycle progression and division. However, filaments formed by wild-type cells upon geldanamycin exposure are quite different in appearance from true hyphae. We have observed that effects on morphology caused by geldanamycin treatment appear to vary in strains with defects in different morphological regulators.

Role of the Fractalkine Receptor in CNS Autoimmune Inflammation: New Approach Utilizing a Mouse Model Expressing the Human CX3CR1 Variant.

Multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS) is the leading cause of non-traumatic neurological disability in young adults. Immune mediated destruction of myelin and oligodendrocytes is considered the primary pathology of MS, but progressive axonal loss is the major cause of neurological disability. In an effort to understand microglia function during CNS inflammation, our laboratory focuses on the fractalkine/CX3CR1 signaling as a regulator of microglia neurotoxicity in various models of neurodegeneration.

Examination of the pathogenic potential of Candida albicans filamentous cells in an animal model of haematogenously disseminated candidiasis.

The opportunistic fungal pathogen Candida albicans is an increasingly common threat to human health. Candida albicans grows in several morphologies and mutant strains locked in yeast or filamentous forms have attenuated virulence in the murine model of disseminated candidiasis. Thus, the ability to change shape is important for virulence.

BRG1 and NRG1 form a novel feedback circuit regulating Candida albicans hypha formation and virulence.

In the opportunistic fungal pathogen Candida albicans both cellular morphology and the capacity to cause disease are regulated by the transcriptional repressor Nrg1p. One of the genes repressed by Nrg1p is BRG1, which encodes a putative GATA family transcription factor. Deletion of both copies of this gene prevents hypha formation.

Candida albicans adhesin Als3p is dispensable for virulence in the mouse model of disseminated candidiasis.

The presence of specific proteins, including Ece1p, Hwp1p and Als3p, distinguishes the Candida albicans hyphal cell wall from that of yeast-form cells. These proteins are thought to be important for the ability of C. albicans cells to adhere to living and non-living surfaces and for the cell-to-cell adhesion necessary for biofilm formation, and also to be pivotal in mediating C.

Pseudohyphal regulation by the transcription factor Rfg1p in Candida albicans.

The opportunistic human fungal pathogen Candida albicans is a major cause of nosocomial infections. One of the fundamental features of C. albicans pathogenesis is the yeast-to-hypha transition.

An analysis of the impact of NRG1 overexpression on the Candida albicans response to specific environmental stimuli.

The ability of the opportunistic fungal pathogen Candida albicans to form filaments has been strongly linked to its capacity to cause disease in humans. We previously described the construction of a strain in which filamentation can be modulated both in vitro and in vivo by placing one copy of the NRG1 gene under the control of a tetracycline-regulatable promoter. To further characterize the role of NRG1 in controlling filamentous growth, and in an attempt to determine whether NRG1 downregulation is a requirement for filamentation per se, or is only necessary under certain environmental conditions, we have conducted an analysis of the growth of the tet-NRG1 strain under a variety of in vitro conditions.

Presence of extracellular DNA in the Candida albicans biofilm matrix and its contribution to biofilms.

DNA has been described as a structural component of the extracellular matrix (ECM) in bacterial biofilms. In Candida albicans, there is a scarce knowledge concerning the contribution of extracellular DNA (eDNA) to biofilm matrix and overall structure. This work examined the presence and quantified the amount of eDNA in C.

Two zinc-cluster transcription factors control induction of alternative oxidase in Neurospora crassa.

The alternative oxidase transfers electrons from ubiquinol to molecular oxygen, providing a mechanism for bypassing the later steps of the standard cytochrome-mediated electron transport chain. The enzyme is found in an array of organisms and in many cases is known to be produced in response to perturbations of the standard chain. Alternative oxidase is encoded in the nucleus but functions in the inner mitochondrial membrane.

Genetic evidence for a regulatory pathway controlling alternative oxidase production in Neurospora crassa.

When the cytochrome-mediated mitochondrial electron transport chain of Neurospora crassa is disrupted, an alternative oxidase encoded by the nuclear aod-1 gene is induced. The alternative oxidase donates electrons directly to oxygen from the ubiquininol pool and is insensitive to chemicals such as antimycin A and KCN that affect the standard electron transport chain. To facilitate isolation of mutants affecting regulation of aod-1, a reporter system containing the region upstream of the aod-1 coding sequence fused to the coding sequence of the N.