Evidence map›Paper›PMID 41833011›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Temporal and Cell-Specific Regulation of Synaptic Homeostasis by the Chromatin Remodeler Chd1.

Danielle T Morency, Tao Cui, Yimei Cai, Chloe Lok, Rachel E Nokku, Ruoxian Huang, Grace L Chu, Yumeng Xie, Saleem W Abu-Tayeh, Kaikai He and 10 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Danielle T MorencyDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.ORCID https://orcid.org/0000-0001-6124-973X
Tao CuiDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.ORCID https://orcid.org/0000-0002-1004-4491
Yimei CaiDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.ORCID https://orcid.org/0000-0003-3716-7800
Chloe LokBiology Department, Georgetown University, Washington, D.C., USA.
Rachel E NokkuBiology Department, Georgetown University, Washington, D.C., USA.
Ruoxian HuangDepartment of Human Science, School of Health, Georgetown University, Washington, D.C., USA.
Grace L ChuBiology Department, Georgetown University, Washington, D.C., USA.
Yumeng XieDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.
Saleem W Abu-TayehDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.
Kaikai HeDepartment of Neurobiology, University of Southern California, Los Angeles, CA, USA.
Chengjie QiuDepartment of Neurobiology, University of Southern California, Los Angeles, CA, USA.
Junyi WangDepartment of Human Science, School of Health, Georgetown University, Washington, D.C., USA.
Paxton M PaganelliDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.
Ting WangDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.
Gabrielle WilliamsDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.
Sreejith NairDepartment of Oncology, Georgetown Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, D.C., USA.
Huadong PeiDepartment of Oncology, Georgetown Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, D.C., USA.
Dion K DickmanDepartment of Neurobiology, University of Southern California, Los Angeles, CA, USA.
Stefano ViciniDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.
Tingting WangDepartment of Pharmacology & Physiology, Georgetown University Medical Center, Washington, D.C., USA.ORCID https://orcid.org/0000-0001-5114-6737

Funding

Generating functional diversity from molecular homogeneity at glutamatergic synapsesR01NS126654 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DION KAI DICKMAN · 2023 to 2026
$1.8M
Stabilizing Brain Function via Glial Epigenetic SignalingR01NS117372 · NINDS · GEORGETOWN UNIVERSITY · PI WANG, TINGTING · 2020 to 2024
$1.8M
Functional Mapping of Chd1-dependent Signaling Network in Synaptic HomeostasisR01MH134978 · NIMH · GEORGETOWN UNIVERSITY · PI Tingting Wang · 2024 to 2026
$1.1M
Matrix Metalloproteinase 2 Controls Trans-Synaptic Homeostatic Plasticity in DrosophilaF31NS139658 · NINDS · GEORGETOWN UNIVERSITY · PI CAI, YIMEI · 2024 to 2025
$78k
Brain and Behavior Research Foundation 27792National Science Foundation 2440057NIH NRSA F31NS139658NIMH NIH HHS R01MH134978NINDS NIH HHS R01NS117372NINDS NIH HHS R01NS126654Simons Foundation Autism Research Initiative 551354Simons Foundation Autism Research Initiative AN-SURFiN-00003291Simons Foundation Autism Research Initiative SFI-AN-SURFiN-00008776Simons Foundation Autism Research Initiative SURFiN-00008126
6 · The paper itself

Abstract

Disruptions in chromatin remodelers and synaptic proteins represent major genetic risk factors for autism spectrum disorder (ASD), yet how these distinct gene classes converge to impair circuit function remains unclear. CHD2, a chromatin remodeler linked to ASD, epilepsy, and intellectual disability, regulates gene expression through epigenetic mechanisms. In Drosophila, its homologue Chd1 functions as a key regulator of presynaptic homeostatic potentiation (PHP), a conserved form of synaptic plasticity that stabilizes neurotransmission. Electrophysiology, calcium imaging, super-resolution microscopy, behavioral assays, and machine learning-based analysis reveal that Chd1 acts in a temporal and cell type-specific manner: it is required in perineurial glia for rapid PHP induction and in motoneurons, muscle, and glia for long-term maintenance. Chd1 controls presynaptic calcium influx and expansion of the readily releasable vesicle pool, both core features of homeostatic compensation. An electrophysiology-based genetic screen guided by unsupervised machine learning identifies 14 Chd1-dependent genes necessary for acute PHP, including the glial-specific effector Cadherin 74A. Loss of Chd1 increases seizure susceptibility and disrupts motor function, mirroring phenotypes observed in CHD2-related neurodevelopmental disorders. These findings establish a mechanistic connection between chromatin remodeling and synaptic homeostasis and identify glial epigenetic regulation as a critical modulator of circuit stability in health and disease.

Indexed as

Autism Spectrum DisorderChromatin Assembly and DisassemblyDNA-Binding ProteinsDrosophila ProteinsHomeostasisNeuronal PlasticitySynapsesAnimalsDrosophilaHumansSynaptic TransmissionDNA-Binding ProteinsDrosophila ProteinsautismChd1epigenetic regulationepilepsyglianeuromuscular junctionpresynaptic homeostatic plasticity

Identifiers

PMID41833011
PMCPMC13271595

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.