Hongkyun Kim
Rosalind Franklin University of Medicine and Science, IL·Neuroscience
Nerve cells pass signals to one another at contact points called synapses. When a signal arrives, calcium flows into the sending cell and triggers the release of chemical messengers called neurotransmitters.
- Fields
Neuroscience
Genetics
Biology
- Topics
CaV2
voltage-gated calcium channels
C. elegans
- Grants
- 2 known grants, through Dec 2030
What they work on
- Test whether a high rate of neurotransmitter release lowers the number of CaV2/UNC-2 calcium channels at C. elegans synapses through negative feedback, using a wide range of mutants that disrupt the release of synaptic vesicles (neurotransmitter-filled sacs).
- Control neuron activity with optogenetic tools (light-switched neurons) and chemical genetic tools to examine how activity sets the level of GFP-tagged UNC-2 channels at the sending end of the synapse.
- Identify the core active zone proteins, the machinery at the neurotransmitter release site, that are required for activity-dependent changes in UNC-2 channel numbers.
- Characterize at the molecular level at least five new genes that a forward genetic screen in C. elegans found to regulate CaV2 channel levels.
- Determine how these newly found genes control the delivery of CaV2 channels to synapses and their breakdown, to reveal possible drug targets for disorders caused by altered channel function.
More about the research
CaV2 channels are the pores in the cell membrane that let this calcium in. Changes in these channel genes are linked to ataxia (loss of movement coordination), seizures and autism. The number of CaV2 channels also rises or falls in many diseases and after injury. However, it is largely unknown how cells deliver these channels to the right place and later break them down. Both projects use the tiny roundworm C. elegans. In this worm each channel part is made by a single gene, which avoids the backup copies found in mammals. Defective channels also cause easy-to-see changes in the worm's rhythmic body movements.
Why it matters
Changes in CaV2 channels are linked to epilepsy, ataxia and autism, and altered homeostatic plasticity is involved in many neurological and psychiatric disorders. Finding the genes and feedback mechanisms that set CaV2 channel levels could reveal new drug targets for raising or lowering channel numbers. This could eventually help in treating conditions caused by altered CaV2 channel function.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Arturo Andrade
Brown University, RI·Neuroscience
Determine how the +18a-CaV2.2 and Δ18a-CaV2.2 calcium channel splice variants affect neurotransmitter release at hippocampal synapses, using electrophysiology in brain slices from mice restricted to one variant.
Mark Alkema
University of Massachusetts Chan Medical School, MA·Neuroscience
Identify the neuronal targets and molecular pathways through which nitric oxide made by gut bacteria suppresses seizures in C. elegans unc-2/CaV2α gain-of-function mutants, a worm model of a migraine-linked calcium channel disorder.
Manu Ben Johny
Columbia University, NY·Biophysics
Determine whether CaV2.1 and CaV2.2 calcium channels are S-palmitoylated, carrying an attached lipid group, in central and peripheral neurons, and how this modification alters channel activity.
The school
Rosalind Franklin University of Medicine and Science: 4 labs on PI Pages, $12M a year on research, 15 research doctorates a year.
More about Rosalind Franklin University of Medicine and Science
Reach out
A start for your email. Fill in the brackets.