Use of stringent selection parameters for the identification of possible selenium-responsive marker genes in mouse liver and gastrocnemius.

Selenium is a trace element that, although toxic in higher concentrations, is essential for human and animal health. In this study, we looked at microarray-based gene expression patterns from liver and gastrocnemius tissues in mice fed either a selenium-deficient diet or diets containing sodium selenite, selenomethionine, or a yeast-derived selenium supplement. A p value cutoff of 0.01 was used to identify a select set of selenium-responsive genes that were consistently differentially expressed across three age groups of mice with both ANOVA and t test analyses. A total of 19 gene transcripts were found to be differentially expressed across the three age groups with at least one selenium-deficient/selenium-supplemented diet comparison. Of those 19 genes, 12 had been previously identified as selenoprotein-encoding genes, and four of the genes, Gpx1, Selh, Sep15, and Sepw1, were differentially expressed in both tissues, all three mouse age groups, and all three diet comparisons. Activities associated with non-selenoproteins encoded by selenium-responsive genes included transport and stress response. The selenophosphate synthetase 2 gene Sephs2 in gastrocnemius tissue and the solute carrier gene Slc48a1 in liver tissue, both up-regulated with selenium-deficient diets compared to all three selenium-supplemented diets, are previously overlooked candidates for dietary selenium marker genes.

SnSAG5 is an alternative surface antigen of Sarcocystis neurona strains that is mutually exclusive to SnSAG1.

Sarcocystis neurona is an obligate intracellular parasite that causes equine protozoal myeloencephalitis (EPM). Previous work has identified a gene family of paralogous surface antigens in S. neurona called SnSAGs. These surface proteins are immunogenic in their host animals, and are therefore candidate molecules for development of diagnostics and vaccines. However, SnSAG diversity exists in strains of S. neurona, including the absence of the major surface antigen gene SnSAG1. Instead, sequence for an alternative SnSAG has been revealed in two of the SnSAG1-deficient strains. Herein, we present data characterizing this new surface protein, which we have designated SnSAG5. The results indicated that the protein encoded by the SnSAG5 sequence is indeed a surface-associated molecule that has characteristics consistent with the other SAGs identified in S. neurona and related parasites. Importantly, Western blot analyses of a collection of S. neurona strains demonstrated that 6 of 13 parasite isolates express SnSAG5 as a dominant surface protein instead of SnSAG1. Conversely, SnSAG5 was not detected in SnSAG1-positive strains. One strain, which was isolated from the brain of a sea otter, did not express either SnSAG1 or SnSAG5. Genetic analysis with SnSAG5-specific primers confirmed the presence of the SnSAG5 gene in Western blot-positive strains, while also suggesting the presence of a novel SnSAG sequence in the SnSAG1-deficient, SnSAG5-deficient otter isolate. The findings provide further indication of S. neurona strain diversity, which has implications for diagnostic testing and development of vaccines against EPM as well as the population biology of Sarcocystis cycling in the opossum definitive host.