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The knockout of Moesin leads to excess microglia-mediated synaptic pruning and impairs social novelty in a mouse

Wanjing Lai1, Junlin Chen2, Hongyao Zhu2

  • 1Key Laboratory of CNS Regeneration (Ministry of Education), Guangdong Key Laboratory of Non-human Primate Research, GHM Institute of CNS Regeneration, Jinan University, Guangzhou, Guangdong 510632, China; School of Biomedical Sciences, The University of Hong Kong, Hong Kong, China.

Cell Reports
|July 17, 2025
PubMed

Insights

A new study reveals that Moesin (Msn) loss in mice leads to autism spectrum disorder (ASD)-like behaviors by affecting interferon signaling and synaptic pruning. This research uncovers a key genetic link between Msn and neurodevelopmental abnormalities.

Area of Science:

  • Neuroscience
  • Genetics
  • Developmental Biology

Background:

  • Genome-wide association studies (GWASs) linked MSNP1AS, an antisense RNA, to autism spectrum disorders (ASDs).
  • MSNP1AS downregulates Moesin (Msn) and is overexpressed in ASD brains, but its in vivo mechanism remained unclear.

Purpose of the Study:

  • To elucidate the functional role of Moesin (Msn) in ASD pathogenesis.
  • To investigate the mechanistic link between Msn loss and ASD-related neurobehavioral traits.

Main Methods:

  • Generation of Msn knockout (KO) mice.
  • Comprehensive neurobehavioral testing in Msn KO mice.
  • Analysis of microglial activation, synaptic pruning, and molecular signaling pathways.

Main Results:

  • Msn KO mice exhibited impaired social novelty and repetitive behaviors, characteristic of ASD.
  • Msn deficiency activated microglia, leading to aberrant C1q-dependent synaptic pruning and medial prefrontal cortex deficits.
  • IFNAR1 antibody treatment rescued microglial abnormalities and social deficits in Msn KO mice.

Conclusions:

  • Moesin (Msn) plays a critical role in mediating interferon signaling and regulating synaptic pruning.
  • Msn deficiency contributes to ASD-like behaviors through aberrant microglial activation and synaptic deficits.
  • This study establishes a functional genetic link between Msn and neurobehavioral abnormalities relevant to ASD.
Keywords:
CP: ImmunologyCP: NeuroscienceMoesininterferonmedial prefrontal cortexmicroglial cellsmousesocial behaviorsynaptic pruning

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