The Arabidopsis outward K+ channel GORK mediates flg22-induced K+ efflux and stomatal closure
- 1The Sainsbury Laboratory
Abstract
Transient K+ efflux occurs rapidly following pathogen-associated molecular pattern (PAMP) perception by pattern recognition receptors (PRRs) as part of pattern-triggered immunity (PTI). However, the molecular identities of the K+ channels responsible for PTI-associated K+ efflux and the mechanisms linking immune signaling to K+ channel regulation remain largely unknown. Here, we show that the channel GUARD CELL OUTWARD RECTIFYING K+ (GORK) is required for K+ efflux and stomatal closure induced by flg22, a model PAMP derived from bacterial flagellin. BOTRYTIS-INDUCED KINASE 1 (BIK1), a receptor-like cytoplasmic kinase associated with immune receptor complexes that functions as a central regulator of PTI, interacts with GORK and phosphorylates the channel on the conserved T199 residue in vitro. Electrophysiological analyses indicate that BIK1 inhibits GORK activity in a kinase-dependent manner and that T199 plays an essential role for GORK function. Together, this study identifies GORK as the key K+ channel executing rapid PTI-associated K+ efflux and associated stomatal closure, thus shedding light on the mechanisms of early immune signaling.
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BibTeX
@misc{wang2026arabidopsis,
title = {{The Arabidopsis outward K+ channel GORK mediates flg22-induced K+ efflux and stomatal closure}},
author = {L. Wang and L. Yue and R. Toth and S. Choi and S. Zhang and T. Maierhofer and S. Snoeck and G. Kim and K. W. Bender and Y. Lee and D. Geiger and T. A. DeFalco and R. Hedrich and C. Zipfel},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.10.758189},
url = {https://www.biorxiv.org/content/10.64898/2026.10.10.758189v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - The Arabidopsis outward K+ channel GORK mediates flg22-induced K+ efflux and stomatal closure
AU - L. Wang
AU - L. Yue
AU - R. Toth
AU - S. Choi
AU - S. Zhang
AU - T. Maierhofer
AU - S. Snoeck
AU - G. Kim
AU - K. W. Bender
AU - Y. Lee
AU - D. Geiger
AU - T. A. DeFalco
AU - R. Hedrich
AU - C. Zipfel
PY - 2026
DA - 2026/10/10
PB - bioRxiv
DO - 10.64898/2026.10.10.758189
UR - https://www.biorxiv.org/content/10.64898/2026.10.10.758189v1
AB - Transient K+ efflux occurs rapidly following pathogen-associated molecular pattern (PAMP) perception by pattern recognition receptors (PRRs) as part of pattern-triggered immunity (PTI). However, the molecular identities of the K+ channels responsible for PTI-associated K+ efflux and the mechanisms linking immune signaling to K+ channel regulation remain largely unknown. Here, we show that the channel GUARD CELL OUTWARD RECTIFYING K+ (GORK) is required for K+ efflux and stomatal closure induced by flg22, a model PAMP derived from bacterial flagellin. BOTRYTIS-INDUCED KINASE 1 (BIK1), a receptor-like cytoplasmic kinase associated with immune receptor complexes that functions as a central regulator of PTI, interacts with GORK and phosphorylates the channel on the conserved T199 residue in vitro. Electrophysiological analyses indicate that BIK1 inhibits GORK activity in a kinase-dependent manner and that T199 plays an essential role for GORK function. Together, this study identifies GORK as the key K+ channel executing rapid PTI-associated K+ efflux and associated stomatal closure, thus shedding light on the mechanisms of early immune signaling.
ER -