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2007)-have been shown to have roles in neuronal migration. 2008), and DYX1C1 on Chr 15 ( Taipale et al. A number of these genes, in specific- DCDC2 and KIAA0319 on Chr 6 ( Francks et al. Recent reports proposing candidate dyslexia susceptibility genes have opened up new lines of investigation into the genetic modulation of this disorder. More recently, an association between periventricular nodular heterotopias and developmental dyslexia has been reported ( Chang et al. Post mortem examination of the brains of developmental dyslexics demonstrated the presence of neuronal migration anomalies, including molecular layer ectopias, laminar dysplasia, and occasional focal microgyria ( Galaburda and Kemper 1979 Galaburda et al.
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The results provide additional supportive evidence linking candidate dyslexia susceptibility genes to migrational disturbances during brain development, and extends the role of Kiaa0319 to include growth and differentiation of dendrites.ĭevelopmental dyslexia is a language–based learning disability that affects between 4% and 10% of the population, and has a strong genetic component ( Fisher and Francks 2006). Neurons transfected with Kiaa0319 shRNA exhibited apical, but not basal, dendrite hypertrophy, which was rescued by overexpression of KIAA0319. In contrast, neurons transfected with the KIAA0319 expression vector attained laminar positions subjacent to their expected positions. Of the Kiaa0319 shRNA–transfected neurons that migrated into the cortical plate, most migrated to their appropriate lamina. This suggested that Kiaa0319 shRNA disrupts neuronal migration by cell autonomous as well as non–cell autonomous mechanisms.
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Knockdown, but not overexpression, of Kiaa0319 resulted in periventricular heterotopias that contained large numbers of both transfected and non–transfected neurons. We used in utero electroporation to transfect cells in E15/16 rat neocortical ventricular zone with either 1) small hairpin RNA (shRNA) vectors targeting Kiaa0319, 2) a KIAA0319 expression construct, 3) Kiaa0319 shRNA along with KIAA0319 expression construct (“rescue”), or 4) a scrambled version of Kiaa0319 shRNA. We investigated the postnatal effects of embryonic knockdown and overexpression of the candidate dyslexia gene homolog Kiaa0319.