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Neuron

Neuron

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ASH1L haploinsufficiency results in autistic-like phenotypes in mice and links Eph receptor gene to autism spectrum disorder

Published:6 April 2022 DOI: 10.1016/j.neuron.2021.12.035 PMID: 35081333
Yuze Yan, Miaomiao Tian, Meng Li, Gang Zhou, Qinan Chen, Mingrui Xu, Yi Hu, Wenhan Luo, Xiuxian Guo, Cheng Zhang, Hong Xie, Qing-Feng Wu, Wei Xiong, Shiguo Liu, Ji-Song Guan

Abstract

ASD-associated genes are enriched for synaptic proteins and epigenetic regulators. How those chromatin modulators establish ASD traits have remained unknown. We find haploinsufficiency of Ash1l causally induces anxiety and autistic-like behavior, including repetitive behavior, and alters social behavior. Specific depletion of Ash1l in forebrain induces similar ASD-associated behavioral defects. While the learning ability remains intact, the discrimination ability of Ash1l mutant mice is reduced. Mechanistically, deletion of Ash1l in neurons induces excessive synapses due to the synapse pruning deficits, especially during the post-learning period. Dysregulation of synaptic genes is detected in Ash1l mutant brain. Specifically, Eph receptor A7 is downregulated in Ash1l+/- mice through accumulating EZH2-mediated H3K27me3 in its gene body. Importantly, increasing activation of EphA7 in Ash1l+/- mice by supplying its ligand, ephrin-A5, strongly promotes synapse pruning and rescues discrimination deficits. Our results suggest that Ash1l haploinsufficiency is a highly penetrant risk factor for ASD, resulting from synapse pruning deficits.

Substances (4)

Materials
Procduct Name CAS Molecular Formula Supplier Price
UNC 1999 1431612-23-5 C33H43N7O2 164 suppliers $14.00-$3876.00
UNC 1999 1431612-23-5 C33H43N7O2 164 suppliers $14.00-$3876.00
UNC 1999 1431612-23-5 C33H43N7O2 164 suppliers $14.00-$3876.00
UNC 1999 1431612-23-5 C33H43N7O2 164 suppliers $14.00-$3876.00

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