A PHD-zinc finger-mediated mechanism for PHF21B recognition of H3K36me3.

Q Ma, J Licinio, M L Wong

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Article in Genomic psychiatry : advancing science from genes to society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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3 authors.

Q MaDepartment of Psychiatry and Behavioral Sciences, College of Medicine, State University of New York, Upstate Medical University, Syracuse, NY 13210, USA.

J LicinioDepartment of Psychiatry and Behavioral Sciences, College of Medicine, State University of New York, Upstate Medical University, Syracuse, NY 13210, USA.

M L WongDepartment of Psychiatry and Behavioral Sciences, College of Medicine, State University of New York, Upstate Medical University, Syracuse, NY 13210, USA.

Funding

Dissecting the roles of an epigenetic regulator of genes involved in synaptic plasticity and social cognition.R01MH127423 · NIMH · UPSTATE MEDICAL UNIVERSITY · PI Julio Licinio, MA-LI WONG · 2022 to 2026

$3.6M

NIMH NIH HHS R01 MH127423

6 · The paper itself

Abstract

HF21B is an epigenetic reader that modulates synaptic plasticity-related genes and social memory (1). Although PHF21B is known to bind H3K36me3, the domain responsible for this interaction has remained uncharacterized. Here, we used co-immunoprecipitation with PHF21B deletion mutants in HEK293T cells to show that the PHD-zinc finger domain is essential for H3K36me3 recognition, whereas the C-terminal coiled-coil region is dispensable. These findings identify the PHD-zinc finger domain as the critical H3K36me3-binding module of PHF21B, with implications for neurological disorders linked to chromosome 22q13.3 deletion, including Phelan-McDermid syndrome (2, 3).

Identifiers

PMID42368242

DOI10.61373/gp026l.0042

PMCPMC13309230

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