RESEARCH ARTICLE


Selenite-Induced Expression of a Caenorhabditis elegans Pro-Aging Factor and Ortholog of Human Selenium-Binding Protein 1



Karl Köhnlein1, 2, #, Nadine Urban1, #, Holger Steinbrenner1, David Guerrero-Gómez3, Antonio Miranda-Vizuete3, Christoph Kaether2, Lars-Oliver Klotz1, *
1 Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich-Schiller-Universität Jena, Jena, Germany;
2 Leibniz Institute on Aging - Fritz Lipmann Institute, Jena, Germany;
3 Instituto de Biomedicina de Sevilla (IBIS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Sevilla, Spain


Copyright: 2020 Lars-Oliver Klotz

* Address correspondence to this author at Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich Schiller University Jena, Dornburger Strasse 29, D-07743 Jena, Germany; Tel: ++49-3641-9-49751; E-mail: lars-oliver.klotz@uni-jena.de# These authors contributed equally.


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.

Keywords: Selenium-binding protein, selenite, stress signaling, Caenorhabditis elegans, lifespan, thioredoxin reductase.




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