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ePoster
CHARACTERIZATION OF AUTISM-ASSOCIATED <EM>DLGAP2/FBXO25 </EM>DOUBLE MUTANT MICE
Odvogmed Bayansanand 2 co-authors
National Taiwan University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-240
Presentation
Date TBA
Board: PS07-10AM-240
Event Information
Poster Board
PS07-10AM-240
Poster
View posterAbstract
Aim: The 8p23.2 chromosomal region is an Autism Spectrum Disorder (ASD) hotspot containing Dlgap2, a postsynaptic scaffolding protein with kinase activity, and Fbxo25, an E3 ubiquitin ligase involved in protein degradation. Our previous studies showed that Dlgap2 knockout mice display behavioral abnormalities—including increased aggression and anxiety, impaired spatial memory, and altered odor perception—along with changes in hippocampal synaptic protein expression and reduced postsynaptic density in the orbitofrontal cortex. Deletion of Fbxo25 also impairs novel object recognition and alters dendritic complexity and postsynaptic protein expression in the hippocampus. Based on these findings, we generated Dlgap2/Fbxo25 double mutant mice to examine the combined effects of these genes on behavior and brain molecular signaling
Methods: Dlgap2/Fbxo25 double mutant mice were generated using CRISPR-Cas9 and assessed using behavioral assays, including open filed and the three-chamber sociability test. Synaptic protein level in the hippocampus was analyzed by Western blot.
Results: Our behavioral analyses revealed normal locomotor activity in double mutant homozygous (Homo) and heterozygous (Het) mice compared with wild-type (WT) mice. The three-chamber sociability test indicated altered sociability in double mutant male mice relative to WT mice. At the molecular level, the postsynaptic scaffolding protein PSD95 was significantly reduced in the hippocampus of Homo and Het male mice compared with mice.
Conclusions: These results suggest that the combined loss of Dlgap2 and Fbxo25 disrupts postsynaptic signaling balance in the hippocampus. Further experiments are required to determine the functional and behavioral consequences of these synaptic alterations and their relevance to ASD-related synaptic dysfunction.
Methods: Dlgap2/Fbxo25 double mutant mice were generated using CRISPR-Cas9 and assessed using behavioral assays, including open filed and the three-chamber sociability test. Synaptic protein level in the hippocampus was analyzed by Western blot.
Results: Our behavioral analyses revealed normal locomotor activity in double mutant homozygous (Homo) and heterozygous (Het) mice compared with wild-type (WT) mice. The three-chamber sociability test indicated altered sociability in double mutant male mice relative to WT mice. At the molecular level, the postsynaptic scaffolding protein PSD95 was significantly reduced in the hippocampus of Homo and Het male mice compared with mice.
Conclusions: These results suggest that the combined loss of Dlgap2 and Fbxo25 disrupts postsynaptic signaling balance in the hippocampus. Further experiments are required to determine the functional and behavioral consequences of these synaptic alterations and their relevance to ASD-related synaptic dysfunction.
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