ArticleTranslational psychiatry2022
Targeted Tshz3 deletion in corticostriatal circuit components segregates core autistic behaviors.
Article in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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7 citing papers in PubMed, 9 citations in OpenAlex.
- Altered striosome-matrix distribution and activity of striatal cholinergic interneurons in a model of autism-linked repetitive behaviors.Molecular psychiatry · 2026Article
- Derepression of transposable elements in the mouse prefrontal cortex disrupts social behavior.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Brain DNA Methylation Atlas of AppAging cell · 2025Article
- Integrating genetics and transcriptomics to characterize shared mechanisms in digestive diseases and psychiatric disorders.Communications biology · 2025Article
- Schizophrenia risk gene ZNF536 modulates retinoic acid response and neuronal gene networks in SH-SY5Y cells.Frontiers in molecular neuroscience · 2025Article
- Heterozygous variants in the teashirt zinc finger homeobox 3 (TSHZ3) gene in human congenital anomalies of the kidney and urinary tract.European journal of human genetics : EJHG · 2025Article
- Developmental deficits of MGE-derived interneurons in theFrontiers in cell and developmental biology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously linked TSHZ3 haploinsufficiency to autism spectrum disorder (ASD) and showed that embryonic or postnatal Tshz3 deletion in mice results in behavioral traits relevant to the two core domains of ASD, namely social interaction deficits and repetitive behaviors. Here, we provide evidence that cortical projection neurons (CPNs) and striatal cholinergic interneurons (SCINs) are two main and complementary players in the TSHZ3-linked ASD syndrome. In the cerebral cortex, TSHZ3 is expressed in CPNs and in a proportion of GABAergic interneurons, but not in cholinergic interneurons or glial cells. In the striatum, TSHZ3 is expressed in all SCINs, while its expression is absent or partial in the other main brain cholinergic systems. We then characterized two new conditional knockout (cKO) models generated by crossing Tshz3
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