Volume 12 Supplement 7

UT-ORNL-KBRIN Bioinformatics Summit 2011

Open Access

Identification of alcohol preference relevant genes in QTL on mouse chromosome 2

  • Lishi Wang1,
  • Yan Jiao1,
  • Griffin Gibson1,
  • Xiaoyun Liu1,
  • Yue Huang1,
  • Beth Bennett2,
  • Kristin Hamre3,
  • Robert Williams3 and
  • Weikuan Gu1Email author
BMC Bioinformatics201112(Suppl 7):A2

DOI: 10.1186/1471-2105-12-S7-A2

Published: 5 August 2011

Background

Previously, a quantitative trait loci (QTL) for alcohol preference on chromosome 2 in a C57BL/6IBG (B6) background has been identified. The overlap of two of interval specific congenic recombinant strains (ISCRS) strains reduced the QTL interval into a 3.4 mbp region.

Results

By using the keyword alcohol, we identified a total of 39 genetic elements in the region between markers D2Mit56 and D2Mit10. Among these genetic elements, we found seven with potential function in alcohol preference (Table 1). We then examined the SNPs, insertions and deletions, and gene expression levels of those seven genes.
Table 1

Candidate genes for alcohol preference on Chr 2.

ENSEMBL ACCESSION

SYMBOL

FULL NAME

SNPS

INSERTIONS

DELETIONS

ENSMUSG00000027104

ATF2

ACTIVATING TRANSCRIPTION FACTOR2

3

  

ENSMUSG00000027109

SP3

TRANS-ACTING TRANSCRIPTION FACTOR3

1(G/A)

 

-

AT(72784944)

ENSMUSG00000006494

PDK1

PYRUVATE DEHYDROGENASE KINASE, ISOENZYME 1

  

-T(71718212)

ENSMUSG00000009207

LNP

LIMB AND NEURAL PATTERNS

9

6

-

TA(74365654)

ENSMUSG00000027107

CHRNA1

CHOLINERGIC RECEPTOR, NICOTINIC, ALPHAPOLYPEPTIDE1

   

ENSMUSG00000018770

ATP5G3

ATP SYNTHASE, H+ TRANSPORTING, MITOCHONDRIAL F0 COMPLEX, SUBUNIT C, (SUBUNIT 9), ISOFORM 3

   

ENSMUSG00000051747

TTN

CONNECTIN

1

  

Conclusions

Our current data suggest that the Atf2 and Titin genes are potentially the most alcohol relevant genes. However, further experiments and examination are still needed to confirm their candidacy. Several other candidate genes are also in the process of being identified.

Declarations

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, TN.

Authors’ Affiliations

(1)
Department of Orthopedic Surgery - Campbell Clinic and Pathology, University of Tennessee Health Science Center
(2)
Department of Pharmacology, University of Colorado Denver
(3)
Department of Anatomy and Neurobiology, University of Tennessee Health Science Center

Copyright

© Wang et al; licensee BioMed Central Ltd. 2011

This article is published under license to 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.

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