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Biotin homeostasis during the cell cycle

Published online by Cambridge University Press:  14 December 2007

Janos Zempleni
Affiliation:
Department of Nutritional Science & Dietetics, University of Nebraska-Lincoln, 316 Ruth Leverton Hall, Lincoln, NE 68583, USA
Donald M Mock*
Affiliation:
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, 4301 W. Markham, Little Rock, AR 72205, USA
*
*Corresponding author: Dr Donald M. Mock, fax +1 501 603 1146, email mockdonaldm@exchange.uams.edu
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Abstract

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Peripheral blood mononuclear cells (PBMC) accumulate biotin by a Na-dependent energy-requiring transporter. This transporter might be the so-called Na-dependent multivitamin transporter, but kinetic observations suggest the existence of a second, more specific, biotin transporter. PBMC respond to proliferation by increased uptake of biotin; the increase is probably mediated by an increased number of transporters on the cell surface. The inferred increase in the biotin transporter synthesis is relatively specific. The increased uptake of biotin into proliferating PBMC is consistent with the hypothesis that these cells have an increased demand for biotin. Indeed, proliferating PBMC increase expression of genes encoding β-methylcrotonyl-CoA carboxylase and propionyl-CoA carboxylase, generating a quantitatively significant increased demand for biotin as a coenzyme in newly-synthesized carboxylases. Moreover, expression of the holocarboxylase synthetase gene increases, consistent with the synthesis of new holocarboxylases. In addition, proliferating PBMC increase both the density of biotinylation of histones and the mass of biotinylated histones per cell, suggesting a potential role for biotin in transcription and replication of DNA.

Type
Research Article
Copyright
Copyright © CABI Publishing 2001

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