Apoptotic proteins reaper and grim induce stable inactivation in voltage-gated K+ channels

V. Avdonin, J. Kasuya, M. A. Ciorba, B. Kaplan, T. Hoshi, L. Iverson

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

Drosophila genes reaper, grim, and head-involution-defective (hid) induce apoptosis in several cellular contexts. N-terminal sequences of these proteins are highly conserved and are similar to N-terminal inactivation domains of voltage-gated potassium (K+) channels. Synthetic Reaper and Grim N terminus peptides induced fast inactivation of Shaker-type K+ channels when applied to the cytoplasmic side of the channel that was qualitatively similar to the inactivation produced by other K+ channel inactivation particles. Mutations that reduce the apoptotic activity of Reaper also reduced the synthetic peptide's ability to induce channel inactivation, indicating that K+ channel inactivation correlated with apoptotic activity. Coexpression of Reaper RNA or direct injection of full length Reaper protein caused near irreversible block of the K+ channels. These results suggest that Reaper and Grim may participate in initiating apoptosis by stably blocking K+ channels.

Original languageEnglish
Pages (from-to)11703-11708
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume95
Issue number20
DOIs
StatePublished - Sep 29 1998

Keywords

  • Apoptosis
  • Drosophila
  • Ion channel
  • Programmed cell death

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