Selenite-induced Expression of a Caenorhabditis elegans Pro-aging Factor and Ortholog of Human Selenium-binding Protein 1

Author:

Köhnlein Karl1ORCID,Urban Nadine1ORCID,Steinbrenner Holger1ORCID,Guerrero-Gómez David2ORCID,Miranda-Vizuete Antonio2ORCID,Kaether Christoph3ORCID,Klotz Lars-Oliver1ORCID

Affiliation:

1. Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich-Schiller-Universität Jena, Jena, Germany

2. Instituto de Biomedicina de Sevilla (IBIS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Sevilla, Spain

3. Leibniz Institute on Aging - Fritz Lipmann Institute, Jena, Germany

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.

Funder

Deutsche Forschungsgemeinschaft

Publisher

Bentham Science Publishers Ltd.

Subject

General Medicine

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