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- Title
Ankyrin B promotes developmental spine regulation in the mouse prefrontal cortex.
- Authors
Murphy, Kelsey E; Duncan, Bryce; Sperringer, Justin E; Zhang, Erin; Haberman, Victoria; Wyatt, Elliott V; Maness, Patricia
- Abstract
Postnatal regulation of dendritic spine formation and refinement in cortical pyramidal neurons is critical for excitatory/inhibitory balance in neocortical networks. Recent studies have identified a selective spine pruning mechanism in the mouse prefrontal cortex mediated by class 3 Semaphorins and the L1 cell adhesion molecules, neuron-glia related cell adhesion molecule, Close Homolog of L1, and L1. L1 cell adhesion molecules bind Ankyrin B, an actin-spectrin adaptor encoded by Ankyrin2 , a high-confidence gene for autism spectrum disorder. In a new inducible mouse model (Nex1Cre-ERT2: Ank2 flox: RCE), Ankyrin2 deletion in early postnatal pyramidal neurons increased spine density on apical dendrites in prefrontal cortex layer 2/3 of homozygous and heterozygous Ankyrin2 -deficient mice. In contrast, Ankyrin2 deletion in adulthood had no effect on spine density. Sema3F-induced spine pruning was impaired in cortical neuron cultures from Ankyrin B-null mice and was rescued by re-expression of the 220 kDa Ankyrin B isoform but not 440 kDa Ankyrin B. Ankyrin B bound to neuron-glia related CAM at a cytoplasmic domain motif (FIGQY1231), and mutation to FIGQH inhibited binding, impairing Sema3F-induced spine pruning in neuronal cultures. Identification of a novel function for Ankyrin B in dendritic spine regulation provides insight into cortical circuit development, as well as potential molecular deficiencies in autism spectrum disorder.
- Publication
Cerebral Cortex, 2023, Vol 33, Issue 20, p10634
- ISSN
1047-3211
- Publication type
Article
- DOI
10.1093/cercor/bhad311