Abscisic acid triggers the endocytosis of the arabidopsis KAT1 K+ channel and its recycling to the plasma membrane

Jens Sutter, Christian Sieben, Andreas Hartel, Cornelia Eisenach, Gerhard Thiel, Michael R Blatt

Research output: Contribution to journalArticle

133 Citations (Scopus)

Abstract

Membrane vesicle traffic to and from the plasma membrane is essential for cellular homeostasis in all eukaryotes. In plants, constitutive traffic to and from the plasma membrane has been implicated in maintaining the population of integral plasma-membrane proteins and its adjustment to a variety of hormonal and environmental stimuli. However, direct evidence for evoked and selective traffic has been lacking. Here, we report that the hormone abscisic acid (ABA), which controls ion transport and transpiration in plants under water stress, triggers the selective endocytosis of the KAT1 K+ channel protein in epidermal and guard cells. Endocytosis of the K+ channel from the plasma membrane initiates in concert with changes in K+ channel activities evoked by ABA and leads to sequestration of the K+ channel within an endosomal membrane pool that recycles back to the plasma membrane over a period of hours. Selective K+ channel endocytosis, sequestration, and recycling demonstrates a tight and dynamic control of the population of K+ channels at the plasma membrane as part of a key plant signaling and response mechanism, and the observations point to a role for channel traffic in adaptive changes in the capacity for osmotic solute flux of stomatal guard cells.
LanguageEnglish
Pages1396-1402
Number of pages7
JournalCurrent Biology
Volume17
Issue number16
DOIs
Publication statusPublished - 21 Aug 2007

Fingerprint

Abscisic Acid
potassium channels
Recycling
endocytosis
Cell membranes
Endocytosis
Arabidopsis
recycling
abscisic acid
plasma membrane
Cell Membrane
traffic
guard cells
Plant Transpiration
Membranes
Transpiration
Ion Transport
Population Dynamics
ion transport
Eukaryota

Keywords

  • cell biology
  • acid triggers
  • abscisic acid

Cite this

Sutter, Jens ; Sieben, Christian ; Hartel, Andreas ; Eisenach, Cornelia ; Thiel, Gerhard ; Blatt, Michael R. / Abscisic acid triggers the endocytosis of the arabidopsis KAT1 K+ channel and its recycling to the plasma membrane. In: Current Biology. 2007 ; Vol. 17, No. 16. pp. 1396-1402.
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Abscisic acid triggers the endocytosis of the arabidopsis KAT1 K+ channel and its recycling to the plasma membrane. / Sutter, Jens; Sieben, Christian; Hartel, Andreas; Eisenach, Cornelia; Thiel, Gerhard; Blatt, Michael R.

In: Current Biology, Vol. 17, No. 16, 21.08.2007, p. 1396-1402.

Research output: Contribution to journalArticle

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T1 - Abscisic acid triggers the endocytosis of the arabidopsis KAT1 K+ channel and its recycling to the plasma membrane

AU - Sutter, Jens

AU - Sieben, Christian

AU - Hartel, Andreas

AU - Eisenach, Cornelia

AU - Thiel, Gerhard

AU - Blatt, Michael R

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AB - Membrane vesicle traffic to and from the plasma membrane is essential for cellular homeostasis in all eukaryotes. In plants, constitutive traffic to and from the plasma membrane has been implicated in maintaining the population of integral plasma-membrane proteins and its adjustment to a variety of hormonal and environmental stimuli. However, direct evidence for evoked and selective traffic has been lacking. Here, we report that the hormone abscisic acid (ABA), which controls ion transport and transpiration in plants under water stress, triggers the selective endocytosis of the KAT1 K+ channel protein in epidermal and guard cells. Endocytosis of the K+ channel from the plasma membrane initiates in concert with changes in K+ channel activities evoked by ABA and leads to sequestration of the K+ channel within an endosomal membrane pool that recycles back to the plasma membrane over a period of hours. Selective K+ channel endocytosis, sequestration, and recycling demonstrates a tight and dynamic control of the population of K+ channels at the plasma membrane as part of a key plant signaling and response mechanism, and the observations point to a role for channel traffic in adaptive changes in the capacity for osmotic solute flux of stomatal guard cells.

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