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Nutrient-Gene Interactions

Diaminobiotin and Desthiobiotin Have Biotin-Like Activities in Jurkat Cells

Rocio Rodriguez-Melendez^*, Brandon Lewis, Robert J. McMahon and Janos Zempleni^*,**,2

Departments of ^* Nutritional Science and Dietetics, and ^** Biochemistry, University of Nebraska at Lincoln, Lincoln, NE and the Center for Nutritional Sciences, Food Science and Human Nutrition Department, University of Florida, Gainesville, FL

²To whom correspondence should be addressed. E-mail: jzempleni2{at}unl.edu.

In mammals, biotin serves as a coenzyme for carboxylases such as propionyl-CoA carboxylase. The expression of genes encoding interleukin-2 (IL-2) and IL-2 receptor (IL-2R) also depends on biotin. Biotin metabolites are structurally similar to biotin, and their concentrations in tissues are quantitatively important. Here, the hypothesis was tested that biotin metabolites can mimic the effects of biotin on gene expression and thus have biotin-like activities. A human T-cell line (Jurkat cells) was used to model effects of biotin and synthetic metabolites (diaminobiotin and desthiobiotin) on the expression of genes encoding IL-2 and IL-2R. Cells were cultured in biotin-deficient medium (0.025 nmol/L biotin) for 35 d; controls were cultured in medium containing 10 nmol/L biotin. The biotin-deficient medium was supplemented with 10 nmol/L of diaminobiotin, desthiobiotin, biotin or no biotin 24 h before gene expression analyses. Transcriptional activities of genes encoding IL-2 and IL-2R were increased up to 43% in cells supplemented with diaminobiotin, desthiobiotin or biotin compared with biotin-deficient cells, as judged by luciferase activities after transfection with reporter-gene constructs. These findings are consistent with the hypothesis that diaminobiotin and desthiobiotin mimic the effects of biotin on gene expression and thus have biotin-like activities. Supplementation of cells with diaminobiotin and desthiobiotin did not affect abundances of holocarboxylases and activities of propionyl-CoA carboxylase, suggesting that effects of synthetic biotin metabolites on gene expression are not mediated by carboxylase-dependent pathways. It is not known whether naturally occurring biotin metabolites also have biotin-like activities.

KEY WORDS: • biotin metabolites • gene expression • humans • interleukin-2 • Jurkat cells

This article has been cited by other articles:

				R. Rodriguez-Melendez and J. Zempleni Nitric Oxide Signaling Depends on Biotin in Jurkat Human Lymphoma Cells J. Nutr., March 1, 2009; 139(3): 429 - 433. [Abstract] [Full Text] [PDF]

				H. M. Pirner and J. Stolz Biotin Sensing in Saccharomyces cerevisiae Is Mediated by a Conserved DNA Element and Requires the Activity of Biotin-Protein Ligase J. Biol. Chem., May 5, 2006; 281(18): 12381 - 12389. [Abstract] [Full Text] [PDF]

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