Differential abscisic acid regulation of guard cell slow anion channels in Arabidopsis wild-type and abi1 and abi2 mutants.

Published

Journal Article

Abscisic acid (ABA) regulates vital physiological responses, and a number of events in the ABA signaling cascade remain to be identified. To allow quantitative analysis of genetic signaling mutants, patch-clamp experiments were developed and performed with the previously inaccessible Arabidopsis guard cells from the wild type and ABA-insensitive (abi) mutants. Slow anion channels have been proposed to play a rate-limiting role in ABA-induced stomatal closing. We now directly demonstrate that ABA strongly activates slow anion channels in wild-type guard cells. Furthermore, ABA-induced anion channel activation and stomatal closing were suppressed by protein phosphatase inhibitors. In abi1-1 and abi2-1 mutant guard cells, ABA activation of slow anion channels and ABA-induced stomatal closing were abolished. These impairments in ABA signaling were partially rescued by kinase inhibitors in abi1 but not in abi2 guard cells. These data provide cell biological evidence that the abi2 locus disrupts early ABA signaling, that abi1 and abi2 affect ABA signaling at different steps in the cascade, and that protein kinases act as negative regulators of ABA signaling in Arabidopsis. New models for ABA signaling pathways and roles for abi1, abi2, and protein kinases and phosphatases are discussed.

Full Text

Duke Authors

Cited Authors

  • Pei, ZM; Kuchitsu, K; Ward, JM; Schwarz, M; Schroeder, JI

Published Date

  • March 1997

Published In

Volume / Issue

  • 9 / 3

Start / End Page

  • 409 - 423

PubMed ID

  • 9090884

Pubmed Central ID

  • 9090884

Electronic International Standard Serial Number (EISSN)

  • 1532-298X

International Standard Serial Number (ISSN)

  • 1040-4651

Digital Object Identifier (DOI)

  • 10.1105/tpc.9.3.409

Language

  • eng