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Papers In Press, published online ahead of print April 1, 2003
Biochemistry, University of Nebraska, Lincoln, NE 68588-0664
Corresponding Author: rbanerjee1{at}unl.edu
Vitamins B12, B6 and folic acid converge at the homocysteine metabolic junction where they support the activities of two key enzymes involved in intracellular homocysteine management, methionine synthase (MS) and cystathionine
J. Biol. Chem, 10.1074/jbc.M300845200
Submitted on January 27, 2003
Revised on April 1, 2003
Accepted on April 1, 2003
Nutritional modulation of gene expression and homocysteine utilization by vitamin B12
-synthase. The molecular mechanism for the regulation of homocysteine metabolism by B12 supplementation has been investigated in this study. B12 supplementation does not alter mRNA or protein turnover rates but induces translational upregulation of MS by shifting the mRNA from the ribonucleoprotein to the polysome pool. The B12 responsive element has been localized by deletion analysis using a reporter gene assay, to a 70 bp region located at the 3' end of the 5´UTR of the MS mRNA. The cellular consequence of the B12 response is a 2- to 3.5-fold increase in the flux of homocysteine through the MS-dependent transmethylation pathway in HepG2 and 293 cells respectively. It is speculated that B
12 induced upregulation of MS may have evolved as an adaptive strategy for rapidly sequestering an essential and rare nutrient whose availability may have been limited in the evolutionary history of mammals, a problem that is exacerbated by the absence of this vitamin from the plant kingdom.
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