ABA and stomatal regulation

Model for ABA signaling in stomatal guard cells. (1) ABA binds to as yet uncharacterized receptor(s). Although shown here on the plasma membrane, there is evidence for both intra- and extra-cellular perception.(2) ABA induces oscillating increases in cytosolic Ca2+ via: -production of reactive oxygen species that contribute to opening of plasma membrane Ca2+in channels -release from internal stores through three types of Ca2+ channels regulated by IP3 (produced by phospholipase C), cyclic ADP-ribose (cADPR), and Ca2+ itself. (3) The increased Ca2+ -inhibits plasma membrane H+ pumps -inhibits K+in channels, and -activates Cl−out (anion) channels, resulting in depolarization of the membrane. (4) Depolarization activates K+out and further inhibits K+in channels.(5) ABA induces PLD-mediated production of phosphatidic acid (PA), which inactivates K+in channels.(6) ABA causes an increase in cytosolic pH which(7) activates K+out channels and inhibits H+ pump activity by depleting the substrate)(8) K+ and anions to be released across the plasma membrane are first released into the cytosol from guard cell vacuoles.The net result is that K+ and anions leave the guard cell, guard cell turgor decreases, and the stomata close. These electrophysiological and volume changes are accompanied by, and require, reorganization of the actin cytoskeleton and at least a two-fold change in plasma membrane surface area.

 

Abscisic acid biosynthesis and response

by Finkelstein R. R., Rock C. D. (2002)

Ruth R. Finkelstein^a,c and Christopher D. Rock^b

^aDepartment of Molecular, Cellular and Developmental Biology, University of California at Santa Barbara, Santa Barbara, CA 93106

^bDepartment of Biological Sciences, Texas Tech University, Lubbock, TX 79409-3131

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In The Arabidopsis Book. Eds. Somerville C.R., Meyerowitz E.M. American Society of Plant Biologists, Rockville, pp 1–52. –

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243367/

INTRODUCTION

Abscisic acid (ABA) is an optically active 15-C weak acid that was first identified in the early 1960s as a growth inhibitor accumulating in abscising cotton fruit (“abscisin II”) and leaves of sycamore trees photoperiodically induced to become dormant (“dormin”) (reviewed in Addicott, 1983). It has since been shown to regulate many aspects of plant growth and development including embryo maturation, seed dormancy, germination, cell division and elongation, and responses to environmental stresses such as drought, salinity, cold, pathogen attack and UV radiation (reviewed in Leung and Giraudat, 1998; Rock, 2000). However, despite the name, it does not appear to control abscission directly; the presence of ABA in abscising organs reflects its role in promoting senescence and/or stress responses, the processes preceding abscission. Although ABA has historically been thought of as a growth inhibitor, young tissues have high ABA levels, and ABA-deficient mutant plants are severely stunted (Figure 1) because their ability to reduce transpiration and establish turgor is impaired. Exogenous ABA treatment of mutants restores normal cell expansion and growth.

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Although the best-characterized aspects of guard cell response are electrophysiological and ultrastructural changes, some of the various ABA response loci have been shown to modify guard-cell specific gene expression. Recent studies have demonstrated that an increase in [Ca²⁺]_cyt, mediates ABA regulated gene expression in guard cells, similar to its role in regulating guard cell turgor (Webb et al., 2001). Of particular interest are the observations that 35S::ABI3 expression acts epistatically to abi1-1 in regulating stomatal aperture (Parcy and Giraudat, 1997), 35S::ABI5 expression enhances stress-induced stomatal closure (Lopez-Molina et al., 2001), and abh1 mutants have altered guard cell expression of a small number of genes (Hugouvieux et al., 2001). Some of the regulatory targets of these transcription factors and CAP-binding protein may play critical roles in stomatal function.