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Spatial component of: CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

ABSTRACT: The gene CELSR3 (cadherin EGF LAG seven‐pass-G‐type receptor 3) has been recently recognized as a high-confidence risk factor for tic disorders (TD). Celsr3 mutant mice displayed tic-like grooming stereotypies and jerks, as well as sensorimotor gating deficits, which were opposed by TD therapies. Spatial transcriptomic analyses revealed that Celsr3 mutants featured abnormalities of the extracellular matrix in the striatum. Notably, there are alterations in collagen and extracellular organization.

ORGANISM(S): Mus musculus

PROVIDER: GSE280709 | GEO | 2025/06/12

REPOSITORIES: GEO

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CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

Project description:The gene CELSR3 (cadherin EGF LAG seven‐pass-G‐type receptor 3) has been recently recognized as a high-confidence risk factor for tic disorders (TD). Celsr3 mutant mice displayed tic-like grooming stereotypies and jerks, as well as sensorimotor gating deficits, which were opposed by TD therapies. Single-nucleus transcriptomic analyses revealed that Celsr3 mutants featured a unique group of eccentric striatal projection neurons. Notably, the Drd3 gene, encoding the dopamine D3 receptor, was significantly upregulated in these cells as well as striosomal D1-positive neurons, while it was reduced in calretinin-positive GABAergic interneurons.

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CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

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Spatial component of: CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

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The chloroplast outer and inner envelope membrane translocase (TOC/TIC) interaction network identifies a 23 kDa glycine-rich protein as new subunit of the 1-MDa TIC complex

Project description:The protein import machinery is essential for chloroplast biogenesis, but knowledge on its exact functioning and the subunits involved in protein translocation is incomplete. Using TAP-tagged Toc159, we reproducibly identified a translocase interaction network that comprises in addition to known TOC members, the 1-MDa TIC complex, six FtsH/FtsHi proteases, Tic110, the KOC1 kinase and several other proteins, some of which with unknown function. The analysis of sub-complexes constituting the Toc159 interaction network in wildtype and a mutant defective in the 1-MDa TIC complex (tic56-3) revealed that the TOC and FtsH/FtsHi complex(es) accumulate independently of the TIC complex as do most other proteins in the network. An exception is a glycine-rich protein of 23 kDa that co-migrates with the 1-MDa complex and is co-regulated with its subunits in tic56-3. This protein was tentatively designated as Tic23. Tic23 abundance is significantly decreased in tic20-I mutant plants and the protein is completely absent from tic56-1 and Spectinomycin-treated wildtype plants lacking Tic214, suggesting a mutual dependency between its accumulation and intactness of the 1-MDa complex. Likewise, tic23-I mutants expressing reduced levels of Tic23 are pale-green and accumulate significantly decreased amounts of Tic20-I. Similar to tic56-3 plastids, the in vitro protein import capacity of tic23-I mutants is not affected. Taken together our results identify Tic23 as an additional component of the 1-MDa TIC complex that is required for complex stability and assembly while it serves complex-mediated functions other than protein import.

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