May 25, 2017 16:00 - 17:30
BSI Central Building 1F Seminar Room
A requirement for de novo protein synthesis is one of the hallmarks of long-lasting synaptic plasticity and long-term memory formation and we, and others, have identified modes of translational control that are required for these processes. Interestingly, mutations in several negative regulators of translation cause syndromes with a high incidence of intellectual disability (ID) and autism spectrum disorder (ASD), including fragile X syndrome (FXS), and we have shown that these alterations in translational control contribute to abnormal synaptic plasticity and aberrant behavior in mice that model FXS and non-syndromic ASD. Moreover, altered translational control also is associated with multiple neurodegenerative diseases, and we have shown that dysregulated translation contributes to synaptic dysfunction and memory impairments in mice that model Alzheimer’s disease (AD). More recently, my laboratory has developed new tools to examine cell-type specific requirements for de novo protein synthesis in memory consolidation, reconsolidation, and extinction. We also have been utilizing translatomics and de novo proteomics to identify the mRNAs that are translated inappropriately in mouse models of ASD and FXS. These studies have revealed interesting links among the activities of translation factors, synaptic plasticity, and memory, and provide insight into the molecular and cellular basis of neurodevelopmental and neurodegenerative disorders.
- Open to Public
- Kazuhiro Yamakawa [Kazuhiro Yamakawa, Neurogenetics ]