As an essential
trace element,
selenium (Se) deficiency results in
White Muscle Disease in livestock and
Keshan disease in humans. The main objectives of this study were to clone and characterize the chicken
selenoprotein W (SeW) gene and investigate SeW
mRNA expression in chicken tissues. The deduced
amino acid (AA) sequence of chicken SeW contains 85 AAs with UAG as the stop
codon. Like all SeW genes identified in different species, chicken SeW contains one well-conserved
selenocysteine (Sec) at the 13th position encoded by the
UGA codon. The proposed
glutathione (GSH)-binding site at the Cys(37) of SeW is not conserved in the chicken, but Cys(9) and Sec(13), with possible GSH binding, are conserved in SeWs identified from all species. There are 23-59% and 50-61% homology in
cDNA and deduced AA sequences of SeW, respectively, between the chicken and other species. The predicted secondary structure of chicken SeW
mRNA indicates that the
selenocysteine insertion sequence element is type II with invariant adenosines within the apical bulge. The SeW
mRNA expression is high in skeletal muscle followed by brain, but extremely low in other tissues from chickens fed a commercial maize-based diet. The SeW gene is ubiquitously expressed in heart, skeletal muscle, brain, testis, spleen, kidney, lung, liver, stomach and pancreas in chickens fed a commercial diet supplemented with
sodium selenite. These results indicate that dietary
selenium supplementation regulates SeW gene expression in the chicken and skeletal muscle is the most responsive tissue when dietary Se content is low.