Abstract:
:The dyslexia-associated gene DCDC2 is 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 Dcdc2 knockout mouse. Comparisons between Dcdc2 knockout mice and wild-type (wt) 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 Dcdc2 knockouts and wild-type mice. Consistent with this hypothesis, we found that deficits in neuronal migration, and dendritic growth caused by RNAi of Dcx were more severe in Dcdc2 knockouts than in wild-type mice with the same transfection. These results indicate that Dcdc2 is not required for neurogenesis, neuronal migration or differentiation in mice, but may have partial functional redundancy with Dcx.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Wang Y,Yin X,Rosen G,Gabel L,Guadiana SM,Sarkisian MR,Galaburda AM,Loturco JJdoi
10.1016/j.neuroscience.2011.06.010subject
Has Abstractpub_date
2011-09-08 00:00:00pages
398-408eissn
0306-4522issn
1873-7544pii
S0306-4522(11)00676-2journal_volume
190pub_type
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