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Related Experiment Video

Updated: Jan 10, 2026

Cell Lineage Analyses and Gene Function Studies Using Twin-spot MARCM

Cell Lineage Analyses and Gene Function Studies Using Twin-spot MARCM

Published on: March 2, 2017

ZMYND11 Restrains KMT2A to Enable a Neuronal Developmental Program.

Alexander W Greben^1,2, Xiaoli S Wu¹, Josephine E Robb¹

¹Department of Neurobiology, Harvard Medical School, Boston, MA, USA.

Biorxiv : the Preprint Server for Biology

|November 24, 2025

Summary

This summary is machine-generated.

Mutations in ZMYND11 cause ZMYND11-related syndromic intellectual disability (ZRSID). Loss of ZMYND11 in neurons disrupts gene expression by inhibiting KMT2A, suggesting KMT2A inhibition as a potential ZRSID therapy.

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Published on: January 12, 2015

Area of Science:

Neuroscience
Genetics
Chromatin Biology

Background:

ZMYND11 mutations cause ZMYND11-related syndromic intellectual disability (ZRSID), characterized by developmental delays and seizures.
Neuronal ZMYND11 loss in mice leads to abnormal gene expression, reduced neuronal connectivity, and behavioral deficits.

Purpose of the Study:

To investigate the mechanism by which ZMYND11 regulates gene expression in the brain.
To explore the therapeutic potential of targeting KMT2A for ZRSID.

Main Methods:

Utilized a ZMYND11 knockout mouse model to study ZRSID.
Investigated ZMYND11's interaction with histone methyltransferase KMT2A (MLL1).
Employed a degron-tagged ZMYND11 mouse model and KMT2A inhibitor revumenib in primary cortical neurons.

Main Results:

ZMYND11 deletion in neurons upregulates non-neuronal gene programs, causing impaired dendritic branching and motor abnormalities.
ZMYND11 directly inhibits KMT2A, a key player in oncogenic and developmental gene programs.
A ZRSID-associated mutation disrupts ZMYND11-KMT2A interaction, highlighting its importance in brain development.
KMT2A inhibition with revumenib attenuated gene expression changes caused by ZMYND11 loss.

Conclusions:

ZMYND11 acts as a crucial regulator of neuronal gene expression by inhibiting KMT2A.
The ZMYND11-KMT2A interaction is vital for normal brain development.
Targeting KMT2A activity presents a potential therapeutic strategy for ZRSID.