ArticleJournal of neurodevelopmental disorders2020
Effects of a postnatal Atrx conditional knockout in neurons on autism-like behaviours in male and female mice.
Article in Journal of neurodevelopmental disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- ATR-X syndrome: genetics, clinical spectrum, and management.Human genetics · 2021Pooled it
- Altered Brain Structure in an ATRX-Deficient Mouse Model of Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2026Article
- Spared cognitive and social function following perinatal ablation of ATRX despite transient microglia dysregulation.Scientific reports · 2026Article
- ATRX function beyond hippocampal CA1 is required for cognitive deficits in mouse models of intellectual disability.PloS one · 2026Article
- Menin Deficiency Induces Autism-Like Behaviors by Regulating Foxg1 Transcription and Participates in Foxg1-Related Encephalopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A mouse model of ATRX deficiency with cognitive deficits and autistic traits.Journal of neurodevelopmental disorders · 2023Article
- Sexually Dimorphic Alterations in the Transcriptome and Behavior with Loss of Histone DemethylaseCells · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
backgroundAlpha-thalassemia/mental retardation, X-linked, or ATRX, is an autism susceptibility gene that encodes a chromatin remodeler. Mutations of ATRX result in the ATR-X intellectual disability syndrome and have been identified in autism spectrum disorder (ASD) patients. The mechanisms by which ATRX mutations lead to autism and autistic-like behaviours are not yet known. To address this question, we generated mice with postnatal Atrx inactivation in excitatory neurons of the forebrain and performed a battery of behavioural assays that assess autistic-like behaviours.
methodsMale and female mice with a postnatal conditional ablation of ATRX were generated using the Cre/lox system under the control of the αCaMKII gene promoter. These mice were tested in a battery of behavioural tests that assess autistic-like features. We utilized paradigms that measure social behaviour, repetitive, and stereotyped behaviours, as well as sensory gating. Statistics were calculated by two-way repeated measures ANOVA with Sidak's multiple comparison test or unpaired Student's t tests as indicated.
resultsThe behaviour tests revealed no significant differences between Atrx-cKO and control mice. We identified sexually dimorphic changes in odor habituation and discrimination; however, these changes did not correlate with social deficits.
conclusionThe postnatal knockout of Atrx in forebrain excitatory neurons does not lead to autism-related behaviours in male or female mice.
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