PUBLICATION

Engineering of a light-gated potassium channel

Authors
Cosentino, C., Alberio, L., Gazzarrini, S., Aquila, M., Romano, E., Cermenati, S., Zuccolini, P., Petersen, J., Beltrame, M., Van Etten, J.L., Christie, J.M., Thiel, G., Moroni, A.
ID
ZDB-PUB-150509-5
Date
2015
Source
Science (New York, N.Y.)   348: 707-10 (Journal)
Registered Authors
Beltrame, Monica
Keywords
none
MeSH Terms
  • Animals
  • Avena/metabolism
  • HEK293 Cells
  • Humans
  • Larva
  • Light
  • Optogenetics*
  • Phototropins/chemistry
  • Phototropins/genetics
  • Potassium Channels/chemistry
  • Potassium Channels/genetics
  • Protein Conformation/radiation effects
  • Protein Engineering
  • Recombinant Fusion Proteins/chemistry
  • Recombinant Fusion Proteins/genetics
  • Recombinant Fusion Proteins/radiation effects*
  • Viral Proteins/chemistry
  • Viral Proteins/genetics
  • Zebrafish
PubMed
25954011 Full text @ Science
Abstract
The present palette of opsin-based optogenetic tools lacks a light-gated potassium (K(+)) channel desirable for silencing of excitable cells. Here, we describe the construction of a blue-light-induced K(+) channel 1 (BLINK1) engineered by fusing the plant LOV2-Jα photosensory module to the small viral K(+) channel Kcv. BLINK1 exhibits biophysical features of Kcv, including K(+) selectivity and high single-channel conductance but reversibly photoactivates in blue light. Opening of BLINK1 channels hyperpolarizes the cell to the K(+) equilibrium potential. Ectopic expression of BLINK1 reversibly inhibits the escape response in light-exposed zebrafish larvae. BLINK1 therefore provides a single-component optogenetic tool that can establish prolonged, physiological hyperpolarization of cells at low light intensities.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping