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- W4384037077 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 (PFC) mediated by class 3 Semaphorins and the L1-CAM cell adhesion molecules Neuron-glia related CAM (NrCAM), Close Homolog of L1 (CHL1), and L1. L1-CAMs bind Ankyrin B (AnkB), an actin-spectrin adaptor encoded by Ankyrin2 ( ANK2 ), a high confidence gene for autism spectrum disorder (ASD). In a new inducible mouse model (Nex1Cre-ERT2: Ank2flox : RCE), Ank2 deletion in early postnatal pyramidal neurons increased spine density on apical dendrites in PFC layer 2/3 of homozygous and heterozygous Ank2 -deficient mice. In contrast, Ank2 deletion in adulthood had no effect on spine density. Sema3F-induced spine pruning was impaired in cortical neuron cultures from AnkB-null mice and was rescued by re-expression of the 220 kDa AnkB isoform but not 440 kDa AnkB. AnkB bound to NrCAM at a cytoplasmic domain motif (FIGQY 1231 ), and mutation to FIGQH inhibited binding, impairing Sema3F-induced spine pruning in neuronal cultures. Identification of a novel function for AnkB in dendritic spine regulation provides insight into cortical circuit development, as well as potential molecular deficiencies in ASD." @default.
- W4384037077 created "2023-07-13" @default.
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- W4384037077 date "2023-07-11" @default.
- W4384037077 modified "2023-10-14" @default.
- W4384037077 title "Ankyrin B Promotes Developmental Spine Regulation in the Mouse Prefrontal Cortex" @default.
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- W4384037077 doi "https://doi.org/10.1101/2023.07.11.548527" @default.
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