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Human Molecular Genetics Advance Access published online on October 3, 2005
Human Molecular Genetics, doi:10.1093/hmg/ddi368
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© The Author 2005. Published by Oxford University Press. All rights reserved
Received August 12, 2005
Revised September 26, 2005
Accepted September 26, 2005

Article

Human MicroRNA (miR-29b) Expression Controls The Amount Of Branched Chain {alpha}-Ketoacid Dehydrogenase Complex In A Cell

Benjamin D. Mersey 1, Peng Jin 1, and Dean J. Danner 2*

1 Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia 30322
2 Department of Human Genetics, Emory University School of Medicine, 615 Michael Street, Room 305C, Atlanta, Georgia 30322

* To whom correspondence should be addressed.
Dean J. Danner, E-mail: ddanner{at}emory.edu


  Abstract

Branched chain amino acids [BCAA] play critical roles in cell and tissue function in addition to being important components of protein structure. The multifunctional roles speak to the need for maintaining tight control of their concentration within cells. Since the BCAA cannot be made de novo in mammals, their cellular concentration is a function of dietary intake, endogenous protein turnover and catabolism of the three amino acids. The branched chain {alpha}-ketoacid dehydrogenase [BCKD] complex commits the BCAA to degradation and thus is vital in controlling their concentration within a cell. In mammals, BCKD activity-state depends on the presence of a covalently bound phosphate on one protein component of the complex. Phosphate is added to the protein through the action of the complex-specific kinase, and results in BCKD inactivation. Here we demonstrate that another reaction plays a role in determining the total amount of BCKD present in a cell. The microRNA (miR29b) molecule tested is targeted to the mRNA for the dihydrolipoamide branched chain acyltransferase component of BCKD and prevents translation when bound. This is the first demonstration of the use of a microRNA to exert control on a metabolic pathway of amino acid catabolism in mammals and offers an explanation for the observed differences in the amount of the BCKD complex present in different tissues and under varying nutritional states.


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