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Sexually dimorphic behavior, neuronal activity, and gene expression in Chd8-mutant mice
Hwajin Jung1, Haram Park2, Yeonsoo Choi2
1Center for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, Korea.
Nature Neuroscience
|August 15, 2018
Summary
A human CHD8 gene mutation causes autism spectrum disorder (ASD) risk. In mice, this mutation leads to distinct behavioral and neural differences between males and females, impacting gene expression and neuronal activity.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Autism spectrum disorders (ASDs) exhibit a significant male prevalence, yet the biological underpinnings remain unclear.
- The CHD8 gene is a crucial chromatin remodeler implicated as a strong risk factor for ASDs.
Purpose of the Study:
- To investigate the impact of a heterozygous Chd8 mutation on behavior and neural function in mice.
- To characterize potential sex-specific differences in response to the Chd8 mutation.
Main Methods:
- Utilized a mouse model with a heterozygous Chd8 mutation (Chd8+/N2373K), mirroring a human ASD-risk variant.
- Assessed behavioral phenotypes across pup, juvenile, and adult stages in both male and female mice.
- Analyzed sexually dimorphic changes in neuronal activity, synaptic transmission, and transcriptomic profiles.
Main Results:
- Male Chd8 mutant mice exhibited abnormal behaviors, including altered vocalizations and social attachment, which were absent in females.
- Females displayed suppressed neuronal excitation and enhanced inhibitory synaptic transmission.
- Transcriptomic analysis revealed sex-specific alterations in gene expression related to extracellular vesicles and the extracellular matrix in females.
Conclusions:
- A human CHD8 mutation induces sexually dimorphic changes in mice, affecting behavior, neuronal function, and gene expression.
- These findings highlight the role of CHD8 in sex-specific neurodevelopmental trajectories relevant to ASDs.
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