Family-based association study of DYX1C1 variants in autism.
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.
Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland. tero.ylisaukko-oja@ktl.fi
Tero
T
Ylisaukko-Oja
Myriam
M
Peyrard-Janvid
Cecilia M
CM
Lindgren
Karola
K
Rehnström
Raija
R
Vanhala
Leena
L
Peltonen
Irma
I
Järvelä
Juha
J
Kere
D000483:Alleles; D001321:Autistic Disorder / Q000235:genetics*; D003598:Cytoskeletal Proteins; D005190:Family; D005260:Female; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D015810:Linkage Disequilibrium; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics*; D009687:Nuclear Proteins / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide
D003598:Cytoskeletal Proteins; C478878:DNAAF4 protein, human; D005819:Genetic Markers; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins