Volume 13 Supplement 12

UT-ORNL-KBRIN Bioinformatics Summit 2012

Open Access

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

  • Fusheng Zhao1, 2,
  • Yonghui Ma1,
  • Yan Jiao1,
  • Lishi Wang1,
  • Yue Huang1,
  • Wei Wei1 and
  • Weikuan Gu1Email author
BMC Bioinformatics201213(Suppl 12):A8

DOI: 10.1186/1471-2105-13-S12-A8

Published: 31 July 2012

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

Ensembl Accession

Symbol

Full Name

ENSMUSG00000039639

Kcne1

potassium voltage-gated channel

ENSMUSG00000022949

CLIC6

Chloride intracellular channel 6

ENSMUSG00000022952

RUNX1

Runt-related transcription factor 1

ENSMUSG00000079514

SLC5A3

Sodium/myo-inositol cotransporter

ENSMUSG00000022982

Sod1

superoxide dismutase 1

ENSMUST00000047383

Kcne2

potassium voltage-gated channel

ENSMUSG00000022967

Ifnar1

interferon (alpha and beta) receptor 1

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.

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, Tennessee.

Authors’ Affiliations

(1)
Department of Orthopedic Surgery-Campbell Clinic and Pathology, University of Tennessee Health Science Center
(2)
Department of Histology and Embryology, Mudanjiang Medical College

Copyright

© Zhao et al; licensee BioMed Central Ltd. 2012

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.

Advertisement