Journal
NEURON
Volume 82, Issue 3, Pages 537-544Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2014.03.015
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Funding
- PBBR Postdoctoral fellowship program (UCSF)
- NIAID [R00 AI085035]
- Howard Hughes Medical Institute
- NINDS [R37 NS40929, R01 NS039313, R01 NS076614]
- NIMH [R00 MH084277]
- Basil O'Connor Starter Scholar Award from the March of Dimes
- Klingenstein Fellowship in Neuroscience
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Ion channel gene expression can vary substantially among neurons of a given type, even though neuron-type-specific firing properties remain stable and reproducible. The mechanisms that modulate ion channel gene expression and stabilize neural firing properties are unknown. In Drosophila, we demonstrate that loss of the Shal potassium channel induces the compensatory rebalancing of ion channel expression including, but not limited to, the enhanced expression and function of Shaker and slowpoke. Using genomic and network modeling approaches combined with genetic and electrophysiological assays, we demonstrate that the transcription factor Kruppel is necessary for the homeostatic modulation of Shaker and slowpoke expression. Remarkably, Kruppel induction is specific to the loss of Shal, not being observed in five other potassium channel mutants that cause enhanced neuronal excitability. Thus, homeostatic signaling systems responsible for rebalancing ion channel expression can be selectively induced after the loss or impairment of a specific ion channel.
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