1. ¹Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland
2. ²Department of Medical Genetics, University of Helsinki, Helsinki, Finland
3. ³Department of Biosciences at Novum Clinical Research Centre, Karolinska Institutet, Huddinge, Sweden
4. ⁴Unit of Child Neurology, Hospital for Children and Adolescents, Helsinki, Finland
5. ⁵Laboratory of Molecular Genetics, HUSLAB, Helsinki, Finland

Correspondence: T Ylisaukko-oja, Department of Molecular Medicine, National Public Health Institute, Biomedicum Helsinki, Haartmaninkatu 8, 00290 Helsinki, Finland. Tel: +358-9-4744 8261; Fax +358-9-4744 8480; E-mail: tero.ylisaukko-oja@ktl.fi

Received 7 May 2004; Revised 1 July 2004; Accepted 6 July 2004; Published online 6 October 2004.

Abstract

DYX1C1 was recently identified as a candidate gene for developmental dyslexia, which is characterized by an unexpected difficulty in learning to read and write despite adequate intelligence, motivation, and education. It will be important to clarify, whether the phenotype caused by DYX1C1 extends to other language-related or comorbid disorders. Impaired language development is one of the essential features in autism. Therefore, we analyzed the allelic distribution of the DYX1C1 gene by family-based association method in 100 Finnish autism families. No evidence for association was observed with any intragenic marker or with haplotypes constructed from alleles of several adjacent markers. No evidence for deviated allelic diversity was either observed: the frequency of expected dyslexia risk haplotype was comparable to its frequency in Finnish controls. Thus it seems unlikely that DYX1C1 gene would be involved in the genetic etiology of autism in Finnish patients.