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Genome-wide copy number scan identifies disruption of PCDH11X in developmental dyslexia

Authors

  • Avinash M. Veerappa,

    1. Genomics Laboratory, Department of Studies in Zoology, University of Mysore, Manasagangotri, Mysore, Karnataka, India
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  • Marita Saldanha,

    1. Department of Studies in Psychology, University of Mysore, Manasagangotri, Mysore, Karnataka, India
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  • Prakash Padakannaya,

    1. Department of Studies in Psychology, University of Mysore, Manasagangotri, Mysore, Karnataka, India
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  • Nallur B. Ramachandra

    Corresponding author
    1. Genomics Laboratory, Department of Studies in Zoology, University of Mysore, Manasagangotri, Mysore, Karnataka, India
    • Correspondence to:

      Prof. Nallur B. Ramachandra, Ph.D., Department of Studies in Zoology, Genomics Laboratory, University of Mysore, Mysore 06, Karnataka, India.

      E-mail: nallurbr@gmail.com

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  • Competing interests statement: The authors declare no competing financial interests.

Abstract

Developmental dyslexia (DD) is a complex heritable disorder with unexpected difficulty in learning to read and spell despite adequate intelligence, education, environment, and normal senses. We performed a whole genome copy number variations (CNV) scan on 11 dyslexic families consisting of 14 dyslexic subjects and 24 non dyslexic members using 1.8 million combined SNP and CNV markers. We found CNVs affecting protocadherin genes in six dyslexics from three families, while none among the non-dyslexic control members showed any CNV in protocadherins. We identified duplications in five cases and a deletion in one case in Xq21.3 region bearing PCDH11X. Unequal recombination between the X-transposed region (XTR) of Yp11.2 and the X chromosome might be causing these structural changes. PCDH11X, expressed in brain is implicated in cell–cell communication, verbal ability, cerebral asymmetry, and dendritic synaptic plasticity, may be regarded as a new candidate gene for dyslexia. © 2013 Wiley Periodicals, Inc.

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