THE DIFFERENTIAL EXPRESSION OF CELL WALL PROTEINS IN THE HUMAN FUNGAL PATHOGEN CANDIDA ALBICANS

Candida albicans is a prevalent opportunistic fungal pathogen which can cause serious diseases from deep mucosal infections to fatal systemic infection. The cell wall of C. albicans is the initial point of interaction with the host during infection and it has an internal polysaccharide layer and an external protein layer. The cell wall proteins are mainly attached to the external layer through GPI anchors and have various functions in nutrient capture, virulence and adhesion. Additionally, the cell wall has three copper-only superoxide dismutases (SOD) SOD4, SOD5 and SOD6 that can protect the yeast from oxidative damage. The rationale for why C. albicans has three unique extracellular SOD enzymes was unknown. Our hypothesis is that each extracellular SOD is expressed under unique environmental conditions, allowing the fungus to survive in many different host niches. To begin to test this hypothesis, we analyzed the expression of the three SODs in comparison to 42 other cell wall proteins by qRT-PCR under four stress conditions differing in metal (iron and copper) content, glucose content and cell morphologies. We found that SOD5 is upregulated in the hyphal morphogenetic state together with some hyphal-induced genes involved in cell adhesion and iron uptake (RBT5, HWP1, ALS3, and HYR1). SOD4 is specifically induced during iron starvation with heme-uptake genes RBT5 and CSA1. The expression of SOD6 is unique and only expressed in yeast-form cells and under iron replete conditions; SOD6 is co-expressed with the adhesion molecule RHD3. The only common pattern with the three SODs is their induction by glucose starvation together with cell wall remodeling genes. In copper starvation, the expression of SODs does not change, although we observe for the first time the induction of heme-uptake genes RBT5, CSA1 and PGA10 with low copper. Overall the three extracellular SODs are induced under very different conditions. Each SOD may be expressed under distinct conditions to protect crucial cell wall proteins from oxidative damage and help C. albicans adapt to different environments in the host

Correcting a major error in assessing organic carbon pollution in natural waters

Microbial degradation of dissolved organic carbon (DOC) in aquatic environments can cause oxygen depletion, water acidification, and CO2 emissions. These problems are caused by labile DOC (LDOC) and not refractory DOC (RDOC) that resists degradation and is thus a carbon sink. For nearly a century, chemical oxygen demand (COD) has been widely used for assessment of organic pollution in aquatic systems. Here, we show through a multicountry survey and experimental studies that COD is not an appropriate proxy of microbial degradability of organic matter because it oxidizes both LDOC and RDOC, and the latter contributes up to 90% of DOC in high-latitude forested areas. Hence, COD measurements do not provide appropriate scientific information on organic pollution in natural waters and can mislead environmental policies. We propose the replacement of the COD method with an optode-based biological oxygen demand method to accurately and efficiently assess organic pollution in natural aquatic environments