Dcdc2 knockout mice display exacerbated developmental disruptions following knockdown of Dcx

Publication year: 2011
Source: Neuroscience, In Press, Accepted Manuscript, Available online 13 June 2011

Yu, Wang , Xiuyin, Yin , Glenn, Rosen , Lisa, Gabel , Sarah M., Guadiana , …

The dyslexia-associated gene DCDC2is a member of the DCX family of genes known to play roles in neurogenesis, neuronal migration and differentiation. Here we report the first phenotypic analysis of a Dcdc2knockout mouse. Comparisons between Dcdc2knockout mice and wild type littermates revealed no significant differences in neuronal migration, neocortical lamination, neuronal cilliogenesis or dendritic differentiation. Considering previous studies showing genetic interactions and potential functional redundancy among members of the DCX family, we tested whether decreasing Dcx expression by RNAi would differentially impair neurodevelopment in Dcdc2knockouts and wild type mice. Consistent with this hypothesis, we found that deficits in neuronal migration,…

▶ We produced the first knockout mouse of Dcdc2. ▶ We find no edivence of neuronal migration disruption in the Dcdc2 mutants. ▶ Dcx RNAi causes a more severe migration deficit in the Dcdc2 mutants. ▶ Dcx RNAi cause a more severe effect on the growth and elaboration of dendrities in the Dcdc2 mutants. ▶ Dcdc2 on its own is not required for neuronal migration in the neocortex, but does render the neocortex more susceptible to migration disruptions caused by Dcx RNAi.