Candida albicans FRE8 encodes a member of the NADPH oxidase family that produces a burst of ROS during fungal morphogenesis.

Until recently, NADPH oxidase (NOX) enzymes were thought to be a property of multicellularity, where the reactive oxygen species (ROS) produced by NOX acts in signaling processes or in attacking invading microbes through oxidative damage. We demonstrate here that the unicellular yeast and opportunistic fungal pathogen Candida albicans is capable of a ROS burst using a member of the NOX enzyme family, which we identify as Fre8. C.

Candida albicans SOD5 represents the prototype of an unprecedented class of Cu-only superoxide dismutases required for pathogen defense.

The human fungal pathogens Candida albicans and Histoplasma capsulatum have been reported to protect against the oxidative burst of host innate immune cells using a family of extracellular proteins with similarity to Cu/Zn superoxide dismutase 1 (SOD1). We report here that these molecules are widespread throughout fungi and deviate from canonical SOD1 at the primary, tertiary, and quaternary levels. The structure of C.

Species-specific activation of Cu/Zn SOD by its CCS copper chaperone in the pathogenic yeast Candida albicans.

Candida albicans is a pathogenic yeast of important public health relevance. Virulence of C. albicans requires a copper and zinc containing superoxide dismutase (SOD1), but the biology of C.

Analysis of hypoxia and hypoxia-like states through metabolite profiling.

Background: In diverse organisms, adaptation to low oxygen (hypoxia) is mediated through complex gene expression changes that can, in part, be mimicked by exposure to metals such as cobalt. Although much is known about the transcriptional response to hypoxia and cobalt, little is known about the all-important cell metabolism effects that trigger these responses.

Methods And Findings: Herein we use a low molecular weight metabolome profiling approach to identify classes of metabolites in yeast cells that are altered as a consequence of hypoxia or cobalt exposures.

Wnt signaling controls the stem cell-like asymmetric division of the epithelial seam cells during C. elegans larval development.

Metazoan stem cells repopulate tissues during adult life by dividing asymmetrically to generate another stem cell and a cell that terminally differentiates. Wnt signaling regulates the division pattern of stem cells in flies and vertebrates. While the short-lived nematode C.

Multiple redundant Wnt signaling components function in two processes during C. elegans vulval development.

In Caenorhabditis elegans, vulval precursor cell (VPC) fate is specified by the action of RTK/Ras, Notch and Wnt signaling pathways. While the identity of signals for the Ras and Notch pathways is known, the source and identity of the Wnt ligand acting on the VPCs are unknown. Single mutations in any of the five Wnt genes (lin-44, cwn-1, cwn-2, egl-20 and mom-2) do not cause strong defects in VPC fate specification, suggesting that functionally redundant Wnts are required.

Identification of cis-regulatory elements from the C. elegans Hox gene lin-39 required for embryonic expression and for regulation by the transcription factors LIN-1, LIN-31 and LIN-39.

Expression of the Caenorhabditis elegans Hox gene lin-39 begins in the embryo and continues in multiple larval cells, including the P cell lineages that generate ventral cord neurons (VCNs) and vulval precursor cells (VPCs). lin-39 is regulated by several factors and by Wnt and Ras signaling pathways; however, no cis-acting sites mediating lin-39 regulation have been identified. Here, we describe three elements controlling lin-39 expression: a 338-bp upstream fragment that directs embryonic expression in P5-P8 and their descendants in the larva, a 247-bp intronic region sufficient for VCN expression, and a 1.

Transcriptional upregulation of the C. elegans Hox gene lin-39 during vulval cell fate specification.

Extracellular signaling pathways and transcriptional regulatory networks function during development to specify metazoan cell fates. During Caenorhabditis elegans vulval development, the specification of three vulval precursor cells (VPCs) requires the activity of Wnt, Notch, and Ras signaling pathways, and function of the Hox gene lin-39. LIN-39 protein levels are regulated in the VPCs by both Wnt and Ras signaling.

Activation of Wnt signaling bypasses the requirement for RTK/Ras signaling during C. elegans vulval induction.

During Caenorhabditis elegans vulval development, activation of receptor tyrosine kinase/Ras and Notch signaling pathways causes three vulval precursor cells (VPCs) to adopt induced cell fates. A Wnt signaling pathway also acts in cell fate specification by the VPCs, via regulation of the Hox gene lin-39. We show here that either mutation of pry-1 or expression of an activated BAR-1 beta-catenin protein causes an Overinduced phenotype, in which greater than three VPCs adopt induced cell fates.