Dcdc2 knockout mice display exacerbated developmental disruptions following knockdown of doublecortin.

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

Neuroscience

journal_title

Neuroscience

authors

Wang Y,Yin X,Rosen G,Gabel L,Guadiana SM,Sarkisian MR,Galaburda AM,Loturco JJ

doi

10.1016/j.neuroscience.2011.06.010

subject

Has Abstract

pub_date

2011-09-08 00:00:00

pages

398-408

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(11)00676-2

journal_volume

190

pub_type

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