Minlab

Our lab is interested in understanding the underlying cellular and molecular networks in normal and dysfunctional neurons affecting distinct brain functions.

To this end, we are working on two projects:

i) Investigate local protein synthesis in neurons that underlies spine morphogenesis and synaptic plasticity.

ii) Identify the cellular and molecular mechanisms of mitochondrial trafficking as well as biogenesis in normal and disease cells.

삼성과제

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● I. To understand the molecular and cellular mechanisms of Intellectual disability.

Scientists do not yet understand how local protein synthesis regulates dendritic spine morphology, a process that is important for learning and memory. Numerous neurological disorders including mental retardation show morphological changes in dendritic spines. Until such understanding is acquired, the molecular link between dysregulation of local protein synthesis and the pathological changes in dendritic spines that lead to intellectual disability will remain largely elusive. Our long-term goal is to better understand the fundamental molecular and cellular mechanisms that underlie cognitive functions. The objective of immediate goal is to determine the underlying molecular mechanisms of local protein synthesis regulating dendritic spine morphology during neuronal stimulation.

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JCB Fig 7 for Wei_Final Image

● II. To investigate mitochondrial dynamics in neurons.

A neuron with extremely polarized structures requires proper distribution and transport of mitochondria in different locations – cell body, axons, and dendrites – in response to physiological needs and synaptic activity. Consequently, defective mitochondrial transport in neurons can cause detrimental effects on neuronal survival and functions. It is widely accepted that the role of mitochondrial anterograde transport from cell body to axon terminals is to provide metabolic energy, while mitochondrial retrograde transport retrieves unhealthy mitochondria from axon terminals or projections and delivers them to the cell body for repair or removal. However, the precise physiological functions of mitochondrial transport in axons have not been adequately investigated. Our long-term goal is to better understand the molecular and cellular mechanisms that underlie mitochondrial dynamics in neurons. The objective of current project is to determine how mitochondrial retrograde transport in axons affects neuronal functions in response to synaptic activity

Rob's paper

그림5