MSL2 disruption leads to autism-like behaviors, impairs neurogenesis, and alters histone H4K16 acetylation

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Impact Factor:6.2

DOI number:10.1007/s00018-026-06237-7

Affiliation of Author(s):中南大学生命科学学院

Teaching and Research Group:医学遗传学

Journal:Cellular and Molecular Life Sciences

Place of Publication:Switzerland

Key Words:Epigenetics; MSL2; Neurodevelopmental disorders; Neurogenesis; Neocortex

Abstract:Neurodevelopmental disorders (NDDs) often involve dysregulated epigenetics, and variants in MSL complex components including MSL2 have been implicated, yet the mechanisms remain unclear. Using nervous-system-specific Msl2 knockout mice and multi-omics profiling, we show that Msl2 deficiency impairs social novelty recognition, learning and memory, with disrupted neocortical lamination and reduced progenitor proliferation and migration. Msl2-deficient brains show reduced H4K16ac and loss of chromatin accessibility at NDD genes, linking MSL2 to chromatin state and neurodevelopment.

Note:JCR Q1，IF 6.2

Co-author:Guodong Chen, Hui Guo, Kun Xia

First Author:Shengjie Luo

Indexed by:Journal Article

Correspondence Author:Shiyi Qu, Senwei Tan, Zhuo Song, Yongqing Lv, Xiangbin Jia, Jieqiong Tan

Discipline:Natural Science

First-Level Discipline:Biology

Document Type:Research Article

Volume:83

Issue:1

Page Number:283

ISSN No.:1420-682X

Translation or Not:no

Date of Publication:2026-05-22