Please cite this article as follows: Brkanac Z, Chapman NH, Matsushita MM, Chun L, Nielsen K, Cochrane E, Berninger VW, Wijsman EM, Raskind WH. 2007. Evaluation of Candidate Genes for DYX1 and DYX2 in Families With Dyslexia. Am J Med Genet Part B 144B:556–560.
Brief Research Communication
Version of Record online: 20 APR 2007
Copyright © 2007 Wiley-Liss, Inc.
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume 144B, Issue 4, pages 556–560, 5 June 2007
How to Cite
Brkanac, Z., Chapman, N. H., Matsushita, M. M., Chun, L., Nielsen, K., Cochrane, E., Berninger, V. W., Wijsman, E. M. and Raskind, W. H. (2007), Evaluation of candidate genes for DYX1 and DYX2 in families with dyslexia. Am. J. Med. Genet., 144B: 556–560. doi: 10.1002/ajmg.b.30471
Zoran Brkanac and Nicola H. Chapman contributed equally to this work.
- Issue online: 24 MAY 2007
- Version of Record online: 20 APR 2007
- Manuscript Accepted: 18 OCT 2006
- Manuscript Received: 31 MAR 2006
- National Institute of Child Health and Development. Grant Numbers: P50 HD33812, K08 HD049342, P30 HD02274
- candidate genes;
- genetic association
Dyslexia is a common heterogeneous disorder with a significant genetic component. Multiple studies have replicated the evidence for linkage between variously defined phenotypes of dyslexia and chromosomal regions on 15q21 (DYX1) and 6p22.2 (DYX2). Based on association studies and the possibility for functional significance of several polymorphisms, candidate genes responsible for the observed linkage signal have been proposed—DYX1C1 for 15q21, and KIAA0319 and DCDC2 for 6p22.2. We investigated the evidence for contribution of these candidate genes to dyslexia in our sample of multigenerational families. Our previous quantitative linkage analyses in this dataset provided supportive evidence for linkage of dyslexia to the locus on chromosome 15, but not to the locus on chromosome 6. In the current study, we used probands from 191 families for a case control analysis, and proband-parent trios for family-based TDT analyses. The observation of weak evidence for transmission disequilibrium for one of the two studied polymorphisms in DYX1C1 suggests involvement of this gene in dyslexia in our dataset. We did not find evidence for the association of KIAA0319 or DCDC2 alleles to dyslexia in our sample. We observed a slight tendency for an intronic deletion in DCDC2 to be associated with worse performance on some quantitative measures of dyslexia in the probands in our sample, but not in their parents. © 2007 Wiley-Liss, Inc.