Removal of a partial genomic duplication restores synaptic transmission and behavior in the MyosinVA mutant mouse Flailer

[1]  F. Bustos,et al.  KMT2C knockout generates ASD-like behaviors in mice , 2023, bioRxiv.

[2]  J. Doudna,et al.  CRISPR technology: A decade of genome editing is only the beginning , 2023, Science.

[3]  K. Rajewsky,et al.  Precise CRISPR-Cas–mediated gene repair with minimal off-target and unintended on-target mutations in human hematopoietic stem cells , 2022, Science advances.

[4]  V. Gradinaru,et al.  Brain-wide Cas9-mediated cleavage of a gene causing familial Alzheimer’s disease alleviates amyloid-related pathologies in mice , 2021, Nature Biomedical Engineering.

[5]  James M. Wilson,et al.  CRISPR/Cas9 directed to the Ube3a antisense transcript improves Angelman syndrome phenotype in mice. , 2021, The Journal of clinical investigation.

[6]  Ramiro D. Almeida,et al.  Myosin Va Brain-Specific Mutation Alters Mouse Behavior and Disrupts Hippocampal Synapses , 2020, eNeuro.

[7]  F. Zhang,et al.  CRISPR-Based Therapeutic Genome Editing: Strategies and In Vivo Delivery by AAV Vectors , 2020, Cell.

[8]  E. Olson,et al.  Enhanced CRISPR-Cas9 correction of Duchenne muscular dystrophy in mice by a self-complementary AAV delivery system , 2020, Science Advances.

[9]  Chang Sik Cho,et al.  CRISPR-Cas9–mediated therapeutic editing of Rpe65 ameliorates the disease phenotypes in a mouse model of Leber congenital amaurosis , 2019, Science Advances.

[10]  Sripriya Ravindra Kumar,et al.  Systemic AAV vectors for widespread and targeted gene delivery in rodents , 2019, Nature Protocols.

[11]  W. Krzyzosiak,et al.  Precise Excision of the CAG Tract from the Huntingtin Gene by Cas9 Nickases , 2018, Front. Neurosci..

[12]  R. Neve,et al.  NMDA receptor subunit composition controls dendritogenesis of hippocampal neurons through CAMKII, CREB‐P, and H3K27ac , 2017, Journal of cellular physiology.

[13]  M. Rots,et al.  Epigenetic editing of the Dlg4/PSD95 gene improves cognition in aged and Alzheimer’s disease mice , 2017, Brain : a journal of neurology.

[14]  Eugene V Koonin,et al.  Diversity, classification and evolution of CRISPR-Cas systems. , 2017, Current opinion in microbiology.

[15]  V. Gradinaru,et al.  Engineered AAVs for efficient noninvasive gene delivery to the central and peripheral nervous systems , 2017, Nature Neuroscience.

[16]  David R. Liu,et al.  CRISPR-Based Technologies for the Manipulation of Eukaryotic Genomes , 2017, Cell.

[17]  S. Jackson,et al.  CRISPR-Cas9D10A nickase-based genotypic and phenotypic screening to enhance genome editing , 2016, Scientific Reports.

[18]  J. Gordon,et al.  Direct Ventral Hippocampal-Prefrontal Input Is Required for Anxiety-Related Neural Activity and Behavior , 2016, Neuron.

[19]  Feng Zhang,et al.  In vivo interrogation of gene function in the mammalian brain using CRISPR-Cas9 , 2014, Nature Biotechnology.

[20]  L. Tsai,et al.  DNA Damage and Its Links to Neurodegeneration , 2014, Neuron.

[21]  N. Inestrosa,et al.  PSD95 Suppresses Dendritic Arbor Development in Mature Hippocampal Neurons by Occluding the Clustering of NR2B-NMDA Receptors , 2014, PloS one.

[22]  Ira M. Hall,et al.  Mosaic Copy Number Variation in Human Neurons , 2013, Science.

[23]  David A. Scott,et al.  Double Nicking by RNA-Guided CRISPR Cas9 for Enhanced Genome Editing Specificity , 2013, Cell.

[24]  G. Church,et al.  CAS9 transcriptional activators for target specificity screening and paired nickases for cooperative genome engineering , 2013, Nature Biotechnology.

[25]  B. van Zundert,et al.  A Myosin Va Mutant Mouse with Disruptions in Glutamate Synaptic Development and Mature Plasticity in Visual Cortex , 2013, The Journal of Neuroscience.

[26]  M. Bennett,et al.  Dysregulation of synaptic plasticity precedes appearance of morphological defects in a Pten conditional knockout mouse model of autism , 2013, Proceedings of the National Academy of Sciences.

[27]  Le Cong,et al.  Multiplex Genome Engineering Using CRISPR/Cas Systems , 2013, Science.

[28]  M. A. Maksimova,et al.  Multiple Autism-Linked Genes Mediate Synapse Elimination via Proteasomal Degradation of a Synaptic Scaffold PSD-95 , 2012, Cell.

[29]  J. Doudna,et al.  A Programmable Dual-RNA–Guided DNA Endonuclease in Adaptive Bacterial Immunity , 2012, Science.

[30]  L. Fagni,et al.  GKAP–DLC2 interaction organizes the postsynaptic scaffold complex to enhance synaptic NMDA receptor activity , 2012, Journal of Cell Science.

[31]  P. Worley,et al.  Disrupted mGluR5-Homer scaffolds mediate abnormal mGluR5 signaling, circuit function and behavior in a mouse model of Fragile X Syndrome , 2012, Nature Neuroscience.

[32]  John A. Hammer,et al.  Walking to work: roles for class V myosins as cargo transporters , 2011, Nature Reviews Molecular Cell Biology.

[33]  B. Sabatini,et al.  Loss of Tsc1 In Vivo Impairs Hippocampal mGluR-LTD and Increases Excitatory Synaptic Function , 2011, The Journal of Neuroscience.

[34]  T. Bourgeron,et al.  Behavioral profiles of mouse models for autism spectrum disorders , 2011, Autism research : official journal of the International Society for Autism Research.

[35]  J. Hammer,et al.  Myosin-Va Transports the Endoplasmic Reticulum into the Dendritic Spines of Purkinje Neurons , 2010, Nature Cell Biology.

[36]  R. Neve,et al.  Differential roles of NMDA Receptor Subtypes NR2A and NR2B in dendritic branch development and requirement of RasGRF1. , 2010, Journal of neurophysiology.

[37]  Robert T. Schultz,et al.  Autism genome-wide copy number variation reveals ubiquitin and neuronal genes , 2009, Nature.

[38]  D. Pinto,et al.  Structural variation of chromosomes in autism spectrum disorder. , 2008, American journal of human genetics.

[39]  Fikret Erdogan,et al.  Array CGH identifies reciprocal 16p13.1 duplications and deletions that predispose to autism and/or mental retardation , 2007, Human mutation.

[40]  Kenny Q. Ye,et al.  Strong Association of De Novo Copy Number Mutations with Autism , 2007, Science.

[41]  Thomas Bourgeron,et al.  Mapping autism risk loci using genetic linkage and chromosomal rearrangements , 2007, Nature Genetics.

[42]  T. Takumi,et al.  Myosin-Va Facilitates the Accumulation of mRNA/Protein Complex in Dendritic Spines , 2006, Current Biology.

[43]  A. El-Husseini,et al.  A Preformed Complex of Postsynaptic Proteins Is Involved in Excitatory Synapse Development , 2006, Neuron.

[44]  P. Donnelly,et al.  A Fine-Scale Map of Recombination Rates and Hotspots Across the Human Genome , 2005, Science.

[45]  G. Hicks,et al.  The RNA Binding Protein TLS Is Translocated to Dendritic Spines by mGluR5 Activation and Regulates Spine Morphology , 2005, Current Biology.

[46]  S. Keeney,et al.  Where the crossovers are: recombination distributions in mammals , 2004, Nature Reviews Genetics.

[47]  M. Moser,et al.  Reduced fear expression after lesions of the ventral hippocampus , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[48]  N. Copeland,et al.  The mouse neurological mutant flailer expresses a novel hybrid gene derived by exon shuffling between Gnb5 and Myo5a. , 2000, Human molecular genetics.

[49]  M. Simon,et al.  A fifth member of the mammalian G-protein beta-subunit family. Expression in brain and activation of the beta 2 isotype of phospholipase C. , 1994, The Journal of biological chemistry.

[50]  D. Witherow,et al.  A Novel Kind of G Protein Heterodimer: The Gβ5-RGS Complex , 2003 .