neuroplasticity in memory & beyond state-of-the-Art genomics

Neuroplasticity serves as the foundation of learning and memory formation, which are indispensable to our lives. Its deficits give rise to an array of disorders, including dementia and post-traumatic stress disorder (PTSD). We will tackle on fundamental questions regarding the epigenetic and transcriptional basis of memory-encoding neuronal ensemble (e.g., engram) formation. To this end, we will employ a multidisciplinary approach that encompasses genomics, mouse genetics, circuit analysis and bioinformatics.

Our laboratory is built upon two main pillars. 

Please also see our research vision regarding the ERC-StG grant (MemoPlasticGenomics)

Epigenetic and transcriptional mechanism regulating IEG inducibility in sensory neurons. t-SNE representation (left) and genome browser view (right) of epigenetic chromatin organization in neuronal activity-response genes at pre-sensory stage (E14.5). In sensory neurons, prior to sensory activity-dependent induction, immediate early genes (IEGs, e.g., Fos, Egr1) are embedded into a unique ‘bipartite' Polycomb chromatin signature. Namely, IEGs carry an active H3K27ac mark on promoters, but a repressive Polycomb-H3K27me3 mark on gene bodies, which is clearly distinct from classic Polycomb bivalent organization that is preferentially found in activity late-response genes (LRGs). Adapted from Kitazawa et al., Nature Genetics 2021.