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

Open Access Meeting abstract

Identification of hearing loss relevant genes in QTL on mouse chromosome 16

Fusheng Zhao12, Yonghui Ma1, Yan Jiao1, Lishi Wang1, Yue Huang1, Wei Wei1 and Weikuan Gu1*

Author Affiliations

1 Department of Orthopedic Surgery-Campbell Clinic and Pathology, University of Tennessee Health Science Center, Memphis, TN 38163, USA

2 Department of Histology and Embryology, Mudanjiang Medical College, Mudanjiang, PR China

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BMC Bioinformatics 2012, 13(Suppl 12):A8  doi:10.1186/1471-2105-13-S12-A8

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2105/13/S12/A8


Published:31 July 2012

© 2012 Zhao 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

Previously, a quantitative trait loci (QTL) for hearing loss on chromosome 16 in a 118 TNE and CAST background has been identified. The overlap of two of interval specific congenic recombinant strains (ISCRS) strains reduced the QTL interval into a 5,378,407 bps genome region.

Results

By examining the genomic information of the QTL on chromosome 16, between the two flanking markers, D16mit191 and D16mit86, we identified a total of 84 genetic elements in the 5,378,407 bps genome region. Among these genetic elements, we found seven with potential function in hearing loss preference (Table 1). We then examined the SNPs, insertions and deletions, and gene expression levels of those seven genes.

Table 1. Candidate genes for hearing loss on Chr 16

Conclusions

Our current data suggest that the Kcne1 and Sod1 genes are potentially the most hearing loss 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.

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.