Email updates

Keep up to date with the latest news and content from BMC Bioinformatics and BioMed Central.

This article is part of the supplement: UT-ORNL-KBRIN Bioinformatics Summit 2012

Open Access Meeting abstract

Evaluation of potential role of Atp5g3 in modulating alcohol preference and obesity

Yue Huang1, Lishi Wang1, Robert W Willliams2, Weikuan Gu1 and Yan Jiao1*

Author affiliations

1 Department of Orthopedic Surgery, University of Tennessee Health Science Center, Memphis, TN 38163, USA

2 Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN 38163, USA

For all author emails, please log on.

Citation and License

BMC Bioinformatics 2012, 13(Suppl 12):A17  doi:10.1186/1471-2105-13-S12-A17


The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2105/13/S12/A17


Published:31 July 2012

© 2012 Huang et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background

Mitochondrial ATP synthase, subunit c, isoform 3 (Atp5g3), encodes subunit 9 of a multisubunit enzyme that catalyzes the synthesis of ATP during oxidative phosphorylation. Each ATP synthase complex has multiple copies of subunit 9 in its transmembrane portion (Fo). While much is known about the molecular mechanisms and function of this complex in the mitochondrial membrane, the impact of variants in this complex and its connection to other pathways and human diseases and disorders is unknown.

Materials and methods

Using extensive phenotype and gene expression data sets in GeneNetwork, we generated correlations between variation in the expression of Atp5g3 in three tissues (hippocampus, cerebellum, and liver) and traits that are related to alcoholism and metabolism/obesity.

Results

With limited numbers of strains, current data in GeneNetwork suggested potential associations between expression levels of Atp5g3 and alcohol and obesity. The expression patterns of Atp5g3 and each of its 12 partner genes/transcripts varied greatly in the same tissue. The correlation in expression levels between Atp5g3 and each of these partners are different in tissues and genes. Transcriptome QTL mapping indicates that the Atp5g3 is differentially regulated in hippocampus, cerebellum, and liver. However, there is currently no reported polymorphism in Atp5g3 and its immediate up- and downstream among three inbred strains—C57BL/6J, DBA/2J, and BALB/cJ.

Conclusions

The potential role of variants in Atp5g3 in both alcoholism and metabolism warrants further investigation. In particular, the focus should be on immediate genetic regulation of Atp5g3 expression and to adduce further evidence to support or refute potential causal links.

Acknowledgments

Support for this research is partially from the NIAAA (1R01 AA016342). NIH, the Veterans Administration Medical Center, and DNA Discovery Core, University of Tennessee, Memphis, Tennessee.