Transcriptomics

Dataset Information

0

Consequences of postnatal Tshz3 deletion: implications for autism spectrum disorder


ABSTRACT: We recently identified heterozygous deletions of the gene TSHZ3, which encodes a Zn-finger transcription factor, in patients with a syndrome including autistic features and provided evidence in mice for a link between Tshz3 haploinsufficiency, defects in cortical projection neurons (CPNs) and autism spectrum disorder (ASD)-like abnormalities. To get more insight into when and where TSHZ3 is required for the proper development of the brain, we generated and characterized a novel mouse model of conditional Tshz3 deletion in projection neurons from postnatal day 2-3 onward. These mice exhibit altered cortical expression of genes encoding for synaptic components, electrophysiological and synaptic changes in layer 5 CPNs, impaired corticostriatal glutamate transmission and plasticity, as well as strong ASD-relevant behavioral deficits. These data, by revealing a crucial postnatal role of TSHZ3 in the development and function of the corticostriatal circuitry that might be determinant for ASD pathogenesis, offer a novel ASD model and further open the possibility for an early postnatal therapeutic window for the syndrome linked to TSHZ3 haploinsufficiency.

ORGANISM(S): Mus musculus

PROVIDER: GSE119791 | GEO | 2021/09/10

REPOSITORIES: GEO

Dataset's files

Source:
Action DRS
Other
Items per page:
1 - 1 of 1

Similar Datasets

2020-09-09 | GSE157658 | GEO
2016-09-26 | GSE85512 | GEO
2022-02-09 | GSE182010 | GEO
2024-02-20 | GSE243662 | GEO
2022-07-21 | GSE203214 | GEO
2022-07-21 | GSE203249 | GEO
2023-05-03 | MSV000091848 | MassIVE
2022-07-21 | GSE189653 | GEO
2024-08-14 | GSE273271 | GEO
2024-08-14 | GSE273270 | GEO