Title:Selenite-induced Expression of a Caenorhabditis elegans Pro-aging Factor and Ortholog of Human Selenium-binding Protein 1
Volume: 1
Author(s): Karl Köhnlein, Nadine Urban, Holger Steinbrenner, David Guerrero-Gómez, Antonio Miranda-Vizuete, Christoph Kaether and Lars-Oliver Klotz*
Affiliation:
- Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich-Schiller-Universität Jena, Jena,Germany
Keywords:
Selenium-binding protein, selenite, stress signaling, Caenorhabditis elegans, lifespan, thioredoxin reductase.
Abstract: Background: The essential trace element and micronutrient selenium exerts most of its
biological actions through incorporation into selenoproteins as selenocysteine. Two further types of
Se-containing proteins exist, including those that have selenomethionine incorporated instead of
methionine, and the group of selenium-binding proteins. We previously described an ortholog of
selenium-binding protein 1 (SELENBP1) in the nematode Caenorhabditis elegans, Y37A1B.5, and
demonstrated that it confers resistance to toxic selenite concentrations while impairing general
stress resistance and life expectancy of C. elegans.
Objective: We tested for the effect of selenite on Y37A1B.5 expression, and we analyzed whether
Y37A1B.5 also shows a lifespan-modulating effect when the nematodes are deficient in the
selenoenzyme thioredoxin reductase-1 (TRXR-1).
Methods: C. elegans expressing a translational reporter construct encoding GFP-tagged Y37A1B.5
under the control of the Y37A1B.5 promoter were exposed to selenite, followed by fluorescence
microscopic analysis of GFP levels. Lifespan analyses and RNA interference experiments were
performed in trxr-1-deficient worms.
Results: We here demonstrate that selenite at toxic concentrations stimulates the expression of the
translational Y37A1B.5 reporter. The lifespan-extending effect of Y37A1B.5 deficiency was
preserved upon the deletion of the only selenoprotein in C. elegans, TRXR-1.
Conclusion: These data suggest that (1) Y37A1B.5 may serve as a selenite-responsive buffer
against high environmental selenium concentrations and that (2) lifespan extension elicited by
Y37A1B.5 knockdown does not require functional TRXR-1.
